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Journal articles on the topic 'Colony Formation Assay'

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Published: 4 June 2021
Last updated: 12 February 2022

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1

Kluin-Nelemans, J. C., H. W. J. Hakvoort, S. E. Boom, E. J. E. G. Bast, and R. Willemze. "Radioresistant pseudo-colony formation in the PHA-leukocyte feeder colony assay." Leukemia Research 12, no. 11-12 (January 1988): 917–22. http://dx.doi.org/10.1016/0145-2126(88)90019-7.

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2

UETSUJI, Yasutomo, Shota FUJIMOTO, Kazuyoshi TSUCHIIYA, and Yoshiaki HIRANO. "Cytotoxicity of Piezoelectric Materials in Colony Formation Assay." Journal of the Society of Materials Science, Japan 58, no. 11 (2009): 943–47. http://dx.doi.org/10.2472/jsms.58.943.

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3

Horman, Shane R., Jeremy To, and Anthony P. Orth. "An HTS-Compatible 3D Colony Formation Assay to Identify Tumor-Specific Chemotherapeutics." Journal of Biomolecular Screening 18, no. 10 (August 5, 2013): 1298–308. http://dx.doi.org/10.1177/1087057113499405.

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There has been increasing interest in the development of cellular behavior models that take advantage of three-dimensional (3D) cell culture. To enable assessment of differential perturbagen impacts on cell growth in 2D and 3D, we have miniaturized and adapted for high-throughput screening (HTS) the soft agar colony formation assay, employing a laser-scanning cytometer to image and quantify multiple cell types simultaneously. The assay is HTS compatible, providing high-quality, image-based, replicable data for multiple, co-cultured cell types. As proof of concept, we subjected colorectal carcinoma colonies in 3D soft agar to a mini screen of 1528 natural product compounds. Hit compounds from the primary screen were rescreened in an HTS 3D co-culture matrix containing colon stromal cells and cancer cells. By combining tumor cells and normal, nontransformed colon epithelial cells in one primary screening assay, we were able to obtain differential IC50 data, thereby distinguishing tumor-specific compounds from general cytotoxic compounds. Moreover, we were able to identify compounds that antagonized tumor colony formation in 3D only, highlighting the importance of this assay in identifying agents that interfere with 3D tumor structural growth. This screening platform provides a fast, simple, and robust method for identification of tumor-specific agents in a biologically relevant microenvironment.
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4

Kajiwara, Yoshinori, Sonali Panchabhai, and Victor A. Levin. "A New Preclinical 3-Dimensional Agarose Colony Formation Assay." Technology in Cancer Research & Treatment 7, no. 4 (August 2008): 329–34. http://dx.doi.org/10.1177/153303460800700407.

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5

Takahashi, Ryo, Nariko Sekine, and Toshihiko Nakatake. "Influence of Monoclonal Antiplatelet Glycoprotein Antibodies on In Vitro Human Megakaryocyte Colony Formation and Proplatelet Formation." Blood 93, no. 6 (March 15, 1999): 1951–58. http://dx.doi.org/10.1182/blood.v93.6.1951.406a33_1951_1958.

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The influence of antiplatelet glycoprotein (GP) antibodies on megakaryocytopoiesis in patients with idiopathic or immune thrombocytopenic purpura (ITP) has been well studied. However, the influence of GP antibodies on proplatelet formation is poorly understood. Here we investigated whether in vitro human megakaryocyte colony formation and proplatelet formation are affected by various monoclonal antiplatelet GP antibodies (MoAb). The megakaryocyte colony formation inhibition assay was performed by methylcellulose culture with modifications, using peripheral blood nonadherent mononuclear cells. The proplatelet formation inhibition assay was performed by megakaryocytes derived from CD34+ cells, stimulated with thrombopoietin + stem cell factor, which were then incubated with antiplatelet GP MoAb for 24 or 48 hours. Anti-GP-Ib MoAb (CD42b; HIP1) slightly inhibited megakaryocyte colony formation (P < .05). and strongly inhibited proplatelet formation (after 24 hours incubation, P < .0002; after 48 hours incubation, P < .0007). Anti-GP-IIb MoAb (CD41; 5B12) inhibited only proplatelet formation (only after 24 hours incubation,P < . 03). Anti-integrin vβ3MoAb (CD51/CD61; 23C6) only slightly inhibited colony size (P < .05). However, anti-GP-IIIa MoAb (CD61; Y2/51) did not inhibit either colony formation or proplatelet formation. These results suggest that antiplatelet GP MoAbs have differing effects on in vitro megakaryocyte colony formation and proplatelet formation.
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6

Dahl, CA, and C. Lindqvist. "Effects of normal mouse serum on the IL-3-induced proliferation of bone marrow cells." Blood 73, no. 3 (February 15, 1989): 700–705. http://dx.doi.org/10.1182/blood.v73.3.700.700.

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Abstract Normal mouse serum (NMS) devoid of colony-stimulating factor (CSF) was found to enhance the interleukin 3 (IL-3)-driven colony formation of bone marrow in vitro. Inclusion of NMS in bone marrow colony-forming assays resulted in greatly increased numbers of colonies and clusters following seven days incubation; however, incubation of bone marrow with NMS before the colony-forming assay had no effect on resultant colony number. The levels of serum-enhancing activity (SEA) did not appear to vary significantly with age and in part was species restricted, in that human and guinea pig serum did not enhance mouse bone marrow colony formation. Conversely, NMS had no effect on human bone marrow colony formation. Levels of SEA were found to vary between strains, as did the degree to which bone marrow from various strains was enhanced by the serum. Serum fractionation studies indicated three active fractions with molecular weights of 800–900 Kd, 60–70 Kd, and 20- 30 Kd. The fraction at 800–900 Kd inhibited colony formation at high concentrations and enhanced colony formation on dilution, whereas the two other active fractions contained enhancing activity at all concentrations tested. These results would indicate that normal serum can play a greater role in colony-forming assays than nutritional supplements. The relationship of the SEA factors to other factors that have been reported to modulate bone marrow colony formation is discussed.
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7

Dahl, CA, and C. Lindqvist. "Effects of normal mouse serum on the IL-3-induced proliferation of bone marrow cells." Blood 73, no. 3 (February 15, 1989): 700–705. http://dx.doi.org/10.1182/blood.v73.3.700.bloodjournal733700.

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Normal mouse serum (NMS) devoid of colony-stimulating factor (CSF) was found to enhance the interleukin 3 (IL-3)-driven colony formation of bone marrow in vitro. Inclusion of NMS in bone marrow colony-forming assays resulted in greatly increased numbers of colonies and clusters following seven days incubation; however, incubation of bone marrow with NMS before the colony-forming assay had no effect on resultant colony number. The levels of serum-enhancing activity (SEA) did not appear to vary significantly with age and in part was species restricted, in that human and guinea pig serum did not enhance mouse bone marrow colony formation. Conversely, NMS had no effect on human bone marrow colony formation. Levels of SEA were found to vary between strains, as did the degree to which bone marrow from various strains was enhanced by the serum. Serum fractionation studies indicated three active fractions with molecular weights of 800–900 Kd, 60–70 Kd, and 20- 30 Kd. The fraction at 800–900 Kd inhibited colony formation at high concentrations and enhanced colony formation on dilution, whereas the two other active fractions contained enhancing activity at all concentrations tested. These results would indicate that normal serum can play a greater role in colony-forming assays than nutritional supplements. The relationship of the SEA factors to other factors that have been reported to modulate bone marrow colony formation is discussed.
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8

Caracciolo, D., N. Shirsat, G. G. Wong, B. Lange, S. Clark, and G. Rovera. "Recombinant human macrophage colony-stimulating factor (M-CSF) requires subliminal concentrations of granulocyte/macrophage (GM)-CSF for optimal stimulation of human macrophage colony formation in vitro." Journal of Experimental Medicine 166, no. 6 (December 1, 1987): 1851–60. http://dx.doi.org/10.1084/jem.166.6.1851.

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Human macrophage colony-stimulating factor (M-CSF or CSF-1), either in purified or in recombinant form, is able to generate macrophagic colonies in a murine bone marrow colony assay, but only stimulates small macrophagic colonies of 40-50 cells in a human bone marrow colony assay. We report here that recombinant human granulocytic/macrophage colony stimulating factor (rhGM-CSF) at concentrations in the range of picograms enhances the responsiveness of bone marrow progenitors to M-CSF activity, resulting in an increased number of macrophagic colonies of up to 300 cells. Polyclonal antiserum against M-CSF did not alter colony formation of bone marrow progenitors incubated with GM-CSF at optimal concentration (1-10 ng/ml) for these in vitro assays. Thus, GM-CSF at higher concentrations (nanogram range) can by itself, elicit macrophagic colonies, and at lower concentrations (picogram range) acts to enhance the responsiveness of these progenitors to M-CSF.
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9

Sedeeq, Mohammed, Ahmed Maklad, Nuri Gueven, and Iman Azimi. "Development of a High-throughput Agar Colony Formation Assay to Identify Drug Candidates against Medulloblastoma." Pharmaceuticals 13, no. 11 (November 5, 2020): 368. http://dx.doi.org/10.3390/ph13110368.

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Medulloblastoma (MB) is the most common malignant childhood brain cancer. High-risk MB tumours have a high incidence of metastasis and result in poor patient survival. Drug screens, commonly used to identify potential novel therapeutic agents against MB, focus on 2D cell proliferation and viability assays given that these assays are easily adaptable to high-throughput regimes. However, 2D models fail to address invasive characteristics that are crucial to MB metastasis and are thus not representative of tumour growth in vivo. In this study, we developed a 3D 384-well agar colony formation assay using MB cells of molecular subgroup 3 that is associated with the highest level of metastasis. Two fluorescence substrates, resazurin and glycyl-phenylalanyl-aminofluorocoumarin (GF-AFC) that measure cell viability via distinct mechanisms were used to assess the growth of MB cells in the agar matrix. The assay was optimised for seeding density, growth period, substrate incubation time and homogeneity of the fluorescent signals within individual wells. Our data demonstrate the feasibility to multiplex the two fluorescent substrates without detectable signal interference. This assay was validated by assessing the concentration-dependent effect of two commonly used chemotherapeutic agents clinically used for MB treatment, vincristine and lomustine. Subsequently, a panel of plasma membrane calcium channel modulators was screened for their effect on the 3D growth of D341 MB cells, which identified modulators of T-type voltage gated and ORAI calcium channels as selective growth modulators. Overall, this 3D assay provides a reproducible, time and cost-effective assay for high-throughput screening to identify potential drugs against MB.
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10

Pragnell, IB, EG Wright, SA Lorimore, J. Adam, M. Rosendaal, JF DeLamarter, M. Freshney, L. Eckmann, A. Sproul, and N. Wilkie. "The effect of stem cell proliferation regulators demonstrated with an in vitro assay." Blood 72, no. 1 (July 1, 1988): 196–201. http://dx.doi.org/10.1182/blood.v72.1.196.196.

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Abstract Spleen colony formation after transplantation of bone marrow cells into irradiated mice has been used as an assay for hematopoietic stem cells (CFU-S), but has serious limitations intrinsic to an in vivo assay. In this report we describe experiments using an in vitro clonogenic assay that is especially suitable for studies of stem cell regulation as defined growth factors and normal untreated bone marrow can be used. We have demonstrated that the colony-forming cells have proliferative properties in common with CFU-S and respond to specific proliferation regulators previously detected using the spleen colony assay.
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11

Pragnell, IB, EG Wright, SA Lorimore, J. Adam, M. Rosendaal, JF DeLamarter, M. Freshney, L. Eckmann, A. Sproul, and N. Wilkie. "The effect of stem cell proliferation regulators demonstrated with an in vitro assay." Blood 72, no. 1 (July 1, 1988): 196–201. http://dx.doi.org/10.1182/blood.v72.1.196.bloodjournal721196.

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Spleen colony formation after transplantation of bone marrow cells into irradiated mice has been used as an assay for hematopoietic stem cells (CFU-S), but has serious limitations intrinsic to an in vivo assay. In this report we describe experiments using an in vitro clonogenic assay that is especially suitable for studies of stem cell regulation as defined growth factors and normal untreated bone marrow can be used. We have demonstrated that the colony-forming cells have proliferative properties in common with CFU-S and respond to specific proliferation regulators previously detected using the spleen colony assay.
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12

KIYOSHIGE, Koji, Hideo UTSUMI, Satoko SHIMBARA, and Akira HAMADA. "Colony Formation Assay Using L-929 Cells to Micropollutants in Water." Journal of Japan Society on Water Environment 15, no. 10 (1992): 748–55. http://dx.doi.org/10.2965/jswe.15.748.

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13

Wylie, Paul G., and Wayne P. Bowen. "Determination of Cell Colony Formation in a High-Content Screening Assay." Clinics in Laboratory Medicine 27, no. 1 (March 2007): 193–99. http://dx.doi.org/10.1016/j.cll.2006.12.008.

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14

WYLIE, P., and W. BOWEN. "Determination of Cell Colony Formation in a High-Content Screening Assay." Journal of the Association for Laboratory Automation 10, no. 4 (August 2005): 203–6. http://dx.doi.org/10.1016/j.jala.2005.06.001.

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15

Zhang, W., J. Tamura, M. Sakuraya, T. Naruse, and K. Kubota. "Effect of Inhibitors of Protein Phosphatase 1 and 2A on Erythroid Colony Formation: An Investigation of the Specificities of Inhibitors." Journal of International Medical Research 29, no. 2 (April 2001): 114–18. http://dx.doi.org/10.1177/147323000102900208.

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To investigate the possible involvement of protein phosphatase (PP)1 and PP2A in the process of erythropoiesis, we assessed the effect of PP1 and PP2A inhibitors on erythroid colony formation using an in vitro colony formation assay. Okadaic acid (OKA), calyculin A (Cal-A) and tautomycin suppressed colony formation but 1-nor-okadaone did not. These results suggest that PP1 and PP2A both play an important role in erythropoiesis. Furthermore, higher concentrations of tautomycin were needed to suppress colony formation compared to concentrations of OKA and Cal-A. The target enzyme of inhibitors in erythropoiesis may be PP2A.
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16

Chen, Xiaoqiang, Chen Li, Wei Chen, Shuchun Lin, Xuehan Yi, Qin Lin, Hao Xu, and Desheng Wang. "Metformin Inhibits the Development of Hypopharyngeal Squamous Cell Carcinoma through Circ_0003214-Mediated MiR-489-3p-ADAM10 Pathway." Journal of Oncology 2021 (July 13, 2021): 1–13. http://dx.doi.org/10.1155/2021/2265475.

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Purpose. This study aims to explore the function of metformin in hypopharyngeal squamous cell carcinoma (HSCC) and the underlying mechanism. Methods. Cell viability, colony formation, cell apoptosis, and cell cycle were investigated using cell counting kit-8 assay, colony formation, and flow cytometry assay. Gene expression was detected by quantitative real-time polymerase chain reaction and western blot. The target relationship was validated by dual-luciferase reporter assay or RNA immunoprecipitation assay. An animal study was implemented to clarify the effect of metformin in vivo. Results. Metformin suppressed HSCC cell viability and colony formation ability and induced cell cycle arrest and apoptosis, and circ_0003214 overexpression weakened these effects. Circ_0003214 regulated A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression via targeting miR-489-3p. Besides, miR-489-3p restoration reversed the role of circ_0003214, and ADAM10 knockdown reversed miR-489-3p inhibition-mediated effect. Moreover, metformin blocked tumor growth via the circ_0003214-miR-489-3p-ADAM10 axis in vivo. Conclusion. Metformin inhibits HSCC progression through the circ_0003214/miR-489-3p/ADAM10 pathway.
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17

Ikhbayar, Khishigdemberel, Nomin Myagmar, Gantulga Davaakhuu, Uyanga Enkhnaran, Enkhmend Bekhbaatar, Jargalan Narmandakh, Oyunsuren Tsendsuren, and Sangaa Deleg. "Evaluation of the Influence of Ferrite Magnetic Nanoparticle for Cancer Cell." Solid State Phenomena 323 (August 30, 2021): 146–51. http://dx.doi.org/10.4028/www.scientific.net/ssp.323.146.

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Magnetic nanoparticles for thermotherapy must be biocompatible and possess high thermal efficiency as heating elements. The biocompatibility of Mg 0.8 Ni 0.2 Fe 2 O 4 nanoparticles was studied using a cytotoxicity colony formation assay and a cell viability assay. HeLa cells exhibited cytotoxic effects when exposed to three different concentrations of 150 μg /ml, 100 μg /ml, and 50 μg /ml nanoparticles. Therefor e, c oncentrations of 50 μg /ml showed the lowest cytotoxic activity and the lowest toxicity to living cells. In vitro cytotoxicity of samples was then investigated by two methods, colony formation assay and cell viability assay. The Hela inhibited cell growth as 16.8% during heating by magnetic field generators.
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18

Liu, Lili, Zhiying Xu, Binbin Yu, Li Tao, and Ying Cao. "Berbamine Inhibits Cell Proliferation and Migration and Induces Cell Death of Lung Cancer Cells via Regulating c-Maf, PI3K/Akt, and MDM2-P53 Pathways." Evidence-Based Complementary and Alternative Medicine 2021 (July 8, 2021): 1–20. http://dx.doi.org/10.1155/2021/5517143.

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Berbamine (BBM) is a natural product isolated from Berberis amurensis Rupr. We investigated the influence of BBM on the cell viability, proliferation, and migration of lung cancer cells and explored the possible mechanisms. The cell viability and proliferation of lung cancer cells were evaluated by MTT assay, EdU assay, and colony formation assay. Migration and invasion abilities of cancer cells were determined through wound scratch assay and Transwell assay. Cell death was evaluated by cell death staining assay and ELISA. The expressions of proteins were evaluated using western blot assay. A xenograft mouse model derived from non-small-cell lung cancer cells was used to detect the effect of BBM on tumor growth and metastasis in vivo. Both colony formation and EdU assays results revealed that BBM (10 μM) significantly inhibited the proliferation of A549 cells ( P < 0.001 ). BBM (10 μM) also significantly inhibited the migration and invasion ability of cancer cells in wound scratch and Transwell assays. Trypan blue assay and ELISA revealed that BBM (20 μM) significantly induced cell death of A549 cells. In xenograft mouse models, the tumor volume was significantly smaller in mice treated with BBM (20 mg/kg). The western blotting assay showed that BBM inhibited the PI3K/Akt and MDM2-p53 signaling pathways, and BBM downregulated the expression of c-Maf. Our results show that BBM inhibits proliferation and metastasis and induces cell death of lung cancer cells in vitro and in vivo. These effects may be achieved by BBM reducing the expression of c-Maf and regulating the PI3K/Akt and MDM2-p53 pathways.
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19

Liu, Tao, Chanji Wu, Guohu Weng, Zhongyan Zhao, Xiangying He, Chuanyi Fu, Zhiyan Sui, and Shi-Xiong Huang. "Bufalin Inhibits Cellular Proliferation and Cancer Stem Cell-Like Phenotypes via Upregulation of MiR-203 in Glioma." Cellular Physiology and Biochemistry 44, no. 2 (2017): 671–81. http://dx.doi.org/10.1159/000485279.

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Background/Aims: Prior studies have shown that bufalin inhibits cellular proliferation and induces apoptosis in various human cancers. MicroRNA-203 (miR-203) has been shown to function as an important regulator of tumor progression at various stages. In this study, we investigated the effect of miR-203 expression and bufalin treatment on glioma cell proliferation and stem cell-like phenotypes. Methods: We used cell viability assay, colony formation assay, cell apoptosis assay and neurosphere formation assay to dectect the treatment effect of bufalin on U251 and U87 cells. Cells were transfected with the miR-203 mimic without bufalin treatment or cells were transfected with anti-miR-203 under bufalin treatment, the above expreiments were repeated. RT-PCR was employed to quantify miR-203 expression. Western blot was performed to detect the stem cell-like (CSC) markers, OCT4 and SOX2. Luciferase activity assay was used to determine whether the SPARC is the target of miR-203. Results: Bufalin treatment inhibited cell proliferation, colony formation, and CSC phenotypes and increased cell apoptosis and expression of miR-203. Furthermore, overexpression of miR-203 led to similar outcomes as bufalin treatment with respect to the cell viability, colony formation, cell apoptosis and the phenotypes of glioma cells. While anti-miR-203 attenuated the inhibitory effects of bufalin as promoting cell proliferation, colony formation and CSC phenotyes and inhibiting cell apoptosis. In addition, we identified SPARC as a novel target gene of miR-203. Conclusions: These findings suggest that miR-203 plays an important role in bufalin’s ability to inhibit the growth of glioma cells and the development of stem cell-like phenotypes.
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20

Hu, Cheng En, Pei Zhun Du, Hui Dong Zhang, and Guang Jian Huang. "Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145." Cellular Physiology and Biochemistry 42, no. 1 (2017): 13–21. http://dx.doi.org/10.1159/000477107.

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Background/Aims: The colorectal neoplasia differentially expressed (CRNDE) gene is a long noncoding RNA (lncRNAs) that is upregulated in colorectal cancer and glioma. Here, we investigated the regulatory function of CRNDE in gastric cancer (GC). Methods: CRNDE and miR-145 expression were assayed by qRT-PCR, and E2F3 protein expression was measured by western blotting. A luciferase reporter assay was used to detect the direct regulation of miR-145 by CRNDE. Cell viability and colony formation of human GC cells were detected using MTT and colony formation assay, respectively. Results: CRNDE was highly expressed in GC cell lines and tissues; overexpression of CRNDE increased GC cell viability and promoted colony formation. Knockdown of CRNDE did not result in loss of expression-related effects on cell proliferation and colony formation. Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145. Conclusion: CRNDE acted as a growth-promoting lncRNA in GC and maybe a potential target of GC treatment.
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21

Donahue, RE, SG Emerson, EA Wang, GG Wong, SC Clark, and DG Nathan. "Demonstration of burst-promoting activity of recombinant human GM-CSF on circulating erythroid progenitors using an assay involving the delayed addition of erythropoietin." Blood 66, no. 6 (December 1, 1985): 1479–81. http://dx.doi.org/10.1182/blood.v66.6.1479.1479.

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Abstract We demonstrate through the use of an in vitro assay involving the delayed addition of erythropoietin that human recombinant GM-CSF, cloned from a mature T cell line, Mo, clearly has burst-promoting activity (BPA) on peripheral blood erythroid progenitors at picomolar concentrations. Delay for up to 72 hours of the addition of erythropoietin to semi-solid methylcellulose cultures of concentrated peripheral blood progenitors minimizes or eliminates BPA-independent erythroid colony formation with little loss of BPA-dependent erythroid colony formation. This assay will prove useful in accurately detecting sources of BPA.
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Donahue, RE, SG Emerson, EA Wang, GG Wong, SC Clark, and DG Nathan. "Demonstration of burst-promoting activity of recombinant human GM-CSF on circulating erythroid progenitors using an assay involving the delayed addition of erythropoietin." Blood 66, no. 6 (December 1, 1985): 1479–81. http://dx.doi.org/10.1182/blood.v66.6.1479.bloodjournal6661479.

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We demonstrate through the use of an in vitro assay involving the delayed addition of erythropoietin that human recombinant GM-CSF, cloned from a mature T cell line, Mo, clearly has burst-promoting activity (BPA) on peripheral blood erythroid progenitors at picomolar concentrations. Delay for up to 72 hours of the addition of erythropoietin to semi-solid methylcellulose cultures of concentrated peripheral blood progenitors minimizes or eliminates BPA-independent erythroid colony formation with little loss of BPA-dependent erythroid colony formation. This assay will prove useful in accurately detecting sources of BPA.
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23

Wu, Yingyong, and Jinyun Peng. "miR-27b Targets HOXB8 to Inhibit Malignant Behaviors of Osteosarcoma." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381987079. http://dx.doi.org/10.1177/1533033819870791.

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MicroRNAs function as either tumor suppressor or oncogene in human cancers. This study aimed to explore the role of miR-27b in osteosarcoma. Expression of miR-27b or homeobox B8 in osteosarcoma cell lines was analyzed by quantitative real-time polymerase chain reaction and Western blot, respectively. Luciferase activity reporter assay and Western blot were conducted to explore the association between miR-27b and homeobox B8. Cell Counting Kit-8, colony formation assay, and wound-healing assay were performed to investigate the role of miR-27b or homeobox B8 on cell proliferation, colony formation, and cell migration. Expression of miR-27b was significantly reduced, while homeobox B8 was increased in osteosarcoma cell lines. In addition, homeobox B8 was validated as a direct target of homeobox B8. Moreover, miR-27b regulates osteosarcoma cell proliferation, colony formation, and migration through targeting homeobox B8. Taken together, our study provides novel insight into the progression of osteosarcoma, and the miR-27b–homeobox B8 axis identified may be developed as therapeutic targets against hepatocellular carcinoma in the future.
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Hosaka, Yoshio, Taiji Tsukamoto, and Michael M. Lieber. "Soft Agarose Colony Formation Assay for Human Renalcell Carcinoma: Comparison of Optical Colony Countingversus Tritiated Thymidine Incorporation." Journal of Urology 136, no. 5 (November 1986): 1102–9. http://dx.doi.org/10.1016/s0022-5347(17)45232-3.

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25

Yamada, Hideto, Emi Kato, Itsuko Furuta, Nobuhiko Hoshi, Kazuki Koizumi, Kenichi Sawada, and Seiichiro Fujimoto. "Hematopoietic Cytokine Levels and In Vitro Colony Formation Assay in Fetal Anemia." Seminars in Thrombosis and Hemostasis 24, no. 05 (October 1998): 485–90. http://dx.doi.org/10.1055/s-2007-996044.

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26

AZECHI, Kazuho, Yasutomo UETSUJI, Kazuyoshi TSUCHIYA, and Yoshiaki HIRANO. "PS5 Cytotoxicity test of Lead-free Piezoelectric Materials in Colony Formation Assay." Proceedings of the Materials and Mechanics Conference 2010 (2010): 12–14. http://dx.doi.org/10.1299/jsmemm.2010.12.

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27

AZECHI, Kazuho, Yasutomo UETSUJI, Kazuyoshi TSUCHIYA, and Yoshiaki HIRANO. "OS0913 Cytotoxicity test of Lead-free Piezoelectric Materials in Colony Formation Assay." Proceedings of the Materials and Mechanics Conference 2011 (2011): _OS0913–1_—_OS0913–3_. http://dx.doi.org/10.1299/jsmemm.2011._os0913-1_.

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28

Lei, Kin Fong, Chich-Hao Kao, and Ngan-Ming Tsang. "High throughput and automatic colony formation assay based on impedance measurement technique." Analytical and Bioanalytical Chemistry 409, no. 12 (March 2, 2017): 3271–77. http://dx.doi.org/10.1007/s00216-017-0270-5.

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29

Ghahremani, Hossein, Majid Sirati-Sabet, and Siamak Salami. "Evaluation of Impacts of Cellular Metabolism on the Migration of Ovarian Cancer Cells by Two in Vitro Assays: A Method Comparison Study." Galen Medical Journal 9 (August 16, 2020): 1831. http://dx.doi.org/10.31661/gmj.v9i0.1831.

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Background: Alteration of metabolic pathways in cancer cells can intensely modulate their migration as an important step in invasion and metastasis. Ketogenic diet showed some contradictory results in cancer patients. In this study the impact of metabolic reprogramming of A2780CP as a model of ovarian cancer stem-like cells on cell migration by two in vitro methods: wound healing and soft agar colony-forming assays. Materials and Methods: short term and long term metabolic reprogramming were done by restriction of glucose to 250mg/L with or without enrichment with beta-hydroxybutyrate (5 milimolar) for 48 hours and 30 days, respectively. Wound healing assay was done and the wound ratio was calculated for 24 and 48 hours. Soft agar colony formation assay was also done in treated and control cells. For method comparison, ten biological replicates were analyzed in triplicate. Results: Migration of A2780CP ovarian cancer stem-like cells were significantly alleviated by long term glucose restriction but no significant changes were observed in short term study. Beta-hydroxybutyrate enrichment did not produce significant impacts on glucose restriction in short or long term studies. Conclusion: The results of colony formation in soft agar and wound or scratch healing assay were in good correlation and convergence which could be used interchangeably in the investigation of metabolic reprogramming in cancer cells. [GMJ.2020;9:e1831]
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30

Yang, Hai, Jiyi Xia, Yan Li, Yong Cao, Li Tang, and Xiaolan Yu. "Baicalein inhibits the invasion of human cervical cancer cells by inhibiting the hedgehog/Gli signaling pathway." Tropical Journal of Pharmaceutical Research 19, no. 1 (April 9, 2020): 115–20. http://dx.doi.org/10.4314/tjpr.v19i1.18.

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Purpose: To identify the role of baicalein in human cervical cancer and to determine whether baicalein treatment affects hedgehog/Gli signaling pathway. Methods: Cell proliferation was evaluated by MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and colony formation assays. Cell death rate was assessed by PI-staining and FACS assay. Furthermore, cell invasion was assessed by Transwell assay while the levels of the key proteins were measured by western blotting analysis. Results: Baicalein suppressed the viability and proliferation of HeLa cells. The colony formation ability and relative migration rate were significantly decreased in the HeLa cells treated with 50 μM baicalein. Furthermore, the levels of Shh, Gli1, MMP-9, and VEGF declined significantly in baicalein-treated cells. Conclusion: The results demonstrate that baicalein inhibits the growth and invasiveness of cervical cancer cells partly by suppressing the activation of hedgehog/Gli signaling pathway in a concentrationdependent manner. Keywords: Cervical cancer, baicalein, hedgehog/Gli pathway, MMP-9
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Jia, Ke-Gang, Gang Feng, Yu-Suo Tong, Guang-Zhou Tao, and Lian Xu. "miR-206 regulates non-small-cell lung cancer cell aerobic glycolysis by targeting hexokinase 2." Journal of Biochemistry 167, no. 4 (November 19, 2019): 365–70. http://dx.doi.org/10.1093/jb/mvz099.

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Abstract Aerobic glycolysis was closely associated with the malignant transformation and prognosis of tumours. miR-206 was found to be downregulated in several cancers. However, whether miR-206 functions in non-small-cell lung cancers (NSCLCs) via the process of aerobic glycolysis remains poorly characterized. Quantitative real-time PCR was performed to detect miR-206 level in NSCLC cells and tissues. The effect of miR-206 on hexokinase 2 (HK2) expression was examined through miR-206 overexpression or miR-206 knockdown. CCK-8 assay and colony formation assay were carried out to explore the role of miR-206 on cell proliferation and colony formation, respectively. The relationship between miR-206 and HK2 was measured by dual-luciferase reporter assay. Glucose consumption, lactate production assay and ATP generation were performed in NSCLC cells following miR-206 and HK2 overexpression. We found that miR-206 was downregulated in NSCLC tissues and cells. miR-206 overexpression downregulated the expression of HK2 via targeting HK2 3′UTR in NSCLC cells. In addition, miR-206 decreased the cell viability and colony formation in NSCLC cells. Furthermore, miR-206 reduced glucose uptake, lactate production and ATP generation in NSCLC cells via HK2 repression. In conclusion, these findings suggested that miR-206 regulated NSCLC cell aerobic glycolysis by targeting HK2.
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Wang, Yiling, Jiantao He, Shenghui Zhang, Qingbo Yang, Bo Wang, Zhiyu Liu, and Xintian Wu. "Knockdown of Immature Colon Carcinoma Transcript 1 Inhibits Proliferation and Promotes Apoptosis of Non–Small Cell Lung Cancer Cells." Technology in Cancer Research & Treatment 16, no. 5 (July 13, 2016): 559–69. http://dx.doi.org/10.1177/1533034616657977.

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Non–small cell lung cancer, as the most frequent type lung cancer, has lower survival rate of 5 years, despite improvements in surgery and chemotherapy. Previous studies showed immature colon carcinoma transcript 1 is closely related to tumorigenesis of human cancer cells. In the present study, we found immature colon carcinoma transcript 1 was overexpressed in lung cancer tissues using Oncomine database mining, and the biological effect of immature colon carcinoma transcript 1 was investigated in non–small cell lung cancer cell lines 95D and A549. Lentivirus-mediated RNA interference was used to knock down immature colon carcinoma transcript 1 expression in 95D and A549 cells in vitro, and the knockdown efficiency was determined using quantitative real-time polymerase chain reaction and Western blot assay. Knockdown of immature colon carcinoma transcript 1 significantly suppressed non–small cell lung cancer cell proliferation and colony formation ability confirmed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Flow cytometry was applied to measure cell cycle arrest, and the result showed the cell cycle arrested in G2/M phase in 95D cells and arrested in G0/G1 phase in A549 cells. Furthermore, we measured the levels of cell cycle–associated proteins by Western blot analysis and found immature colon carcinoma transcript 1 –mediated cell proliferation inhibition appeared due to downregulation of cell cycle activator cyclin D1 and upregulation of cell cycle inhibitor p21. In addition, immature colon carcinoma transcript 1 silencing significantly induced non–small cell lung cancer cell apoptosis by annexin V/7-amino-actinomycin D double-staining assay. All our data suggest that immature colon carcinoma transcript 1 may play an important role for non–small cell lung cancer cell proliferation and could be a potential molecular target for diagnosing and treating human non–small cell lung cancer.
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Wang, Maohua, Jian Xie, Yong Fu, Yongchun Zhou, and Maohua Wang. "Silencing of cluster determinant 36 transmitted by gold nanoparticles inhibits the occurrence and progression of breast cancer by down-regulating the peroxisome proliferative activated receptor signaling pathway." Materials Express 11, no. 5 (May 1, 2021): 789–800. http://dx.doi.org/10.1166/mex.2021.1981.

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Breast cancer is the most commonly diagnosed tumor in women worldwide. Although a range of therapeutic strategies have been developed in recent years, the outcome for patients is often poor. The purpose of this study was to explore the molecular mechanisms of the membrane glycoprotein CD36 in breast cancer. Cells from breast cancer cell lines were transfected with gold nanoparticles protected by liposomes, as gene vectors. Cell counting kit 8 assays were performed to determine cell variability, EdU straining assays were used to evaluate cell proliferation, and colony formation assays were performed to detect cell colony ability. The number of cells involved in migration and invasion was counted using Transwell assays. Lymphangiogenesis formation was assessed using lymphangiogenesis formation assay. Xenograft tumor mice were established, to analyze the effects of CD36. Quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry (IHC) were performed to estimate the expression of genes. Silencing of CD36 inhibited cell variability, proliferation, colony formation, lymphangiogenesis, and repressed cell migration and invasion in vitro. Overexpression of PPAR reversed the effects of the silencing of CD36, and the effects of PPAR upregulation were blocked by PPAR inhibitor. In vivo, tumor growth and lymphangiogenesis and PPAR activation were suppressed by the silencing of CD36. Silencing of CD36 also inhibited the variability, proliferation, colony formation, lymphangiogenesis, migration and invasion of breast cancer cells by suppressing PPAR signaling pathway activation. The CD36 gene was transfected with gold nanoparticles which improved the efficiency of gene transfection. The use of gold nanoparticles provides a new way to study the effects of genes on tumor cells.
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Du, Rina, Pengwei Zhao, Shikui Wu, Yaoxing Gao, Rina Wu, Minli Yang, Wanying Song, and Haining Gao. "Sendeng-4 Suppressed Melanoma Growth by Induction of Autophagy and Apoptosis." Evidence-Based Complementary and Alternative Medicine 2021 (August 23, 2021): 1–10. http://dx.doi.org/10.1155/2021/5519973.

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Sendeng-4 is a traditional Chinese medicine that has been successfully applied to anti-inflammatory diseases in clinical practice. Monomers within Sendeng-4 showed promising antitumor activity against lung cancer, colon cancer, and cutaneous cancer. However, potency of Sendeng-4 in melanoma has not been explored. This study aims to explore the potential application of Sendeng-4 in melanoma treatment. In the present study, we systemically investigate the possibility of Sendeng-4 for treatment of melanoma cancer in vitro by proliferation assay, colony formation, flow cell cytometry, RNA-seq, western blot, and fluorescence-based assay. Our data demonstrated that Sendeng-4 suppresses the proliferation and colony formation capacity of melanoma cells and induces cell cycle block at G2/M phase and eventually cell death. Mechanistically, transcriptome sequencing demonstrates that the PI3K-AKT pathway was significantly inactivated upon Sendeng-4 exposure, which was confirmed by western blot showing decreased phosphorylation of AKT. In addition, decreased BCL-2 expression and increased BAX expression were observed, suggesting programmed cell death via apoptosis. Moreover, LC3-II production as well as autophagosomes formation was observed as demonstrated by western blot and immunofluorescence, indicating elevated autophagy network by Sendeng-4 stimulation. Collectively, we concluded that Sendeng-4 might be used as an anticancer drug for melanoma.
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Xu, Shan, Haibao Zhang, Tianjie Liu, Wenjie Yang, Wei Lv, Dalin He, Peng Guo, and Lei Li. "6-Gingerol induces cell-cycle G1-phase arrest through AKT–GSK 3β–cyclin D1 pathway in renal-cell carcinoma." Cancer Chemotherapy and Pharmacology 85, no. 2 (December 12, 2019): 379–90. http://dx.doi.org/10.1007/s00280-019-03999-9.

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Abstract Purpose 6-Gingerol, a major biochemical and pharmacological active ingredient of ginger, has shown anti-inflammatory and antitumor activities against various cancers. Searching for natural products with fewer side effects for developing adjunctive therapeutic options is necessary. Methods The effects of 6-gingerol on proliferation, colony formation, and cell cycle in RCC cells were detected by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, and propidium iodide (PI) staining, respectively. Western blotting, an immunofluorescence assay, and immunohistochemical staining were performed to assess the expression of relevant proteins. A subcutaneous tumor model was set up to investigate the 6-gingerol effects on tumor growth in vivo, and the pharmacokinetics of 6-gingerol in mice were detected by LC/MS assays. Results 6-Gingerol treatment exerted time- and dose-dependent inhibition of the growth and colony formation of ACHN, 786-O, and 769-P cells, leading to a concomitant induction of cell-cycle G1-phase arrest and decrease in Ki-67 expression in the cell nucleus. Western-blotting results showed that 6-gingerol reduces phosphorylation of protein kinase B (AKT) Ser 473, cyclin-dependent kinases (CDK4), and cyclin D1 and, meanwhile, increases glycogen synthase kinase (GSK 3β) protein amount. Furthermore, the efficacy of 6-gingerol was demonstrated in an in vivo murine model of 786-O. Conclusion The above results indicate that 6-gingerol can induce cell-cycle arrest and cell-growth inhibition through the AKT–GSK 3β–cyclin D1 signaling pathway in vitro and in vivo, suggesting that 6-gingerol should be useful for renal-cell carcinoma treatment.
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Matsui, T., T. Oike, E. Nuryadi, and T. Nakano. "Inter-Study Precision of Cancer Cell Radiosensitivity As Assessed By Colony Formation Assay." International Journal of Radiation Oncology*Biology*Physics 105, no. 1 (September 2019): E671. http://dx.doi.org/10.1016/j.ijrobp.2019.06.978.

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Zheng, Li, Jiangtao Chen, Zhongyong Zhou, and Zhikuan He. "Knockdown of long non-coding RNA HOXD-AS1 inhibits gastric cancer cell growth via inactivating the JAK2/STAT3 pathway." Tumor Biology 39, no. 5 (May 2017): 101042831770533. http://dx.doi.org/10.1177/1010428317705335.

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Long non-coding RNA HOXD-AS1 (HOXD cluster antisense RNA 1) has been demonstrated to be closely associated with the progression of several tumors. However, the biological function of HOXD-AS1 and the underlying molecular mechanism in gastric cancer are still unclear. The expression of HOXD-AS1 in gastric cancer cell lines was evaluated by quantitative real-time polymerase chain reaction. The association of HOXD-AS1 expression and clinical parameters was statistically analyzed by chi-square test. Cell viability, colony formation capacity, and phosphorylation of Janus kinase 2 and signal transducer and activator of transcription 3 in treated SGC-7901 and BGC-823 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay, and western blot analysis, respectively. The results indicated that HOXD-AS1 was significantly upregulated in gastric cancer cells and clinically involved in tumor size, invasion depth, tumor–node–metastasis stages, regional lymph nodes, lymphatic metastasis, as well as distant metastasis. HOXD-AS1 knockdown dramatically inhibited gastric cancer cell proliferation, colony formation capacity, and phosphorylation of Janus kinase 2 and signal transducer and activator of transcription 3 in vitro. In addition, HOXD-AS1 overexpression significantly promoted gastric cancer cell proliferation and colony formation capacity, whereas both Janus kinase small interfering RNAs and Janus kinase 2 inhibitor AG490 overturned these effects. Furthermore, xenograft assays confirmed the biological function of HOXD-AS1 in vivo. Taken together, our data elucidate that knockdown of HOXD-AS1 dramatically suppresses gastric cancer cell growth by inactivating the Janus kinase 2/signal transducer and activator of transcription 3 pathway in vitro and in vivo, contributing to a better understanding of gastric cancer pathogenesis and providing a possible theoretical foundation for long non-coding RNA–directed diagnosis and therapy against this disease.
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Wang, Zhenshi, Jiaolong Wang, Zhihua Chen, Kun Wang, and Lianshui Shi. "MicroRNA-1-3p inhibits the proliferation and migration of oral squamous cell carcinoma cells by targeting DKK1." Biochemistry and Cell Biology 96, no. 3 (June 2018): 355–64. http://dx.doi.org/10.1139/bcb-2017-0015.

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We investigated the functional role and mechanism of miR-1-3p and DKK1 in oral squamous cell carcinoma (OSCC) cells. The level of miR-1-3p and DKK1 expression were detected in OSCC tissues and cells using reverse-transcription – quantitative PCR and Western blot. A dual luciferase reporter gene assay was applied to confirm the targeting relationship between miR-1-3p and DKK1. Functional assays, including MTT, Transwell, colony formation, and flow cytometry analysis were conducted to verify their effect on cell progressions. MTT, colony formation, and Transwell assays indicated that the proliferation, migration, and invasion of SCC-4 cells was impaired with high miR-1-3p expression but promoted with high DKK1 expression. The results from cell cycle analysis and annexin-V–PI assays for apoptosis suggested that miR-1-3p suppressed the transit of SCC-4 cells from G0/G1 to S and induced apoptosis. In summary, miR-1-3p suppressed the progression of OSCC by inhibiting DKK1 expression.
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Kwon, Young Jik, Gene Hung, W. French Anderson, Ching-An Peng, and Hong Yu. "Determination of Infectious Retrovirus Concentration from Colony-Forming Assay with Quantitative Analysis." Journal of Virology 77, no. 10 (May 15, 2003): 5712–20. http://dx.doi.org/10.1128/jvi.77.10.5712-5720.2003.

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ABSTRACT The colony formation assay is the most commonly used titration method for defining the concentration of replication-incompetent murine leukemia virus-derived retroviral vectors. However, titer varies with target cell type and number, transduction time, and concentration of polycation (e.g., Polybrene). Moreover, because most of the viruses cannot encounter target cells due to Brownian motion, their short half-lives, and the requirement for target cell division for activity, the actual infectious retrovirus concentration in the collected supernatant is higher than the viral titer. Here we correlate the physical viral particle concentration with the infectious virus concentration and colony formation titer with the help of a mathematical model. Ecotropic murine leukemia retrovirus supernatant, collected from the GP+E86/LNCX retroviral vector producer cell line, was concentrated by centrifugation and further purified by a sucrose density gradient. The physical concentration of purified viral vectors was determined by direct particle counting with an electron microscope. The concentrations of fresh and concentrated supernatant were determined by a quantitative reverse transcriptase activity assay. Titration of all supernatants by neomycin-resistant colony formation assay was also performed. There were 767 ± 517 physical viral particles per infectious CFU in the crude viral supernatant. However, the infectious viral concentration determined by mathematical simulation was 143 viral particles per infectious unit, which is more consistent with the concentration determined by particle counting in purified viral solution. Our results suggest that the mathematical model can be used to extract a more accurate and reliable concentration of infectious retrovirus.
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Heyworth, CM, TM Dexter, SE Nicholls, and AD Whetton. "Protein kinase C activators can interact synergistically with granulocyte colony-stimulating factor or interleukin-6 to stimulate colony formation from enriched granulocyte-macrophage colony-forming cells." Blood 81, no. 4 (February 15, 1993): 894–900. http://dx.doi.org/10.1182/blood.v81.4.894.894.

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Abstract The effects of direct activators of protein kinase C (PKC) (the phorbol ester tetradecanoyl phorbol myristic acid [TPA] or bryostatin) on the ability of a highly enriched population of granulocyte-macrophage colony-forming cells (GM-CFC) to proliferate and develop in soft agar was assessed. In the absence of colony stimulating factors, the PKC activators did not stimulate colony formation. However, in the presence of optimal concentrations of granulocyte colony-stimulating factor (G- CSF) or interleukin-6 (IL-6), TPA or bryostatin markedly elevated the number of colonies formed from the GM-CFC. In the absence of TPA, IL-6, and G-CSF, respectively, both stimulated the formation of about 3% of the colonies observed when IL-3 was present. When TPA plus G-CSF or IL- 6 were added together, this figure increased to 48% and 54%, respectively. In both instances, the types of mature cells formed was altered from colonies of mature neutrophilic cells to a mixture consisting predominantly of macrophages with some neutrophils. Similar results were observed when bryostatin replaced TPA in these assays. When single cell colony-forming assays were performed, the same results were obtained. The presence of G-CSF, or IL-6, and the activator of PKC used (TPA or bryostatin) was required throughout the colony-forming assay for an optimal synergistic effect to be observed. These data indicate that agents that activate PKC can promote the proliferation and development of GM-CFC via a synergistic interaction with G-CSF or IL-6. Furthermore, there is an apparent role for PKC in development and possibly lineage commitment of GM-CFC.
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Heyworth, CM, TM Dexter, SE Nicholls, and AD Whetton. "Protein kinase C activators can interact synergistically with granulocyte colony-stimulating factor or interleukin-6 to stimulate colony formation from enriched granulocyte-macrophage colony-forming cells." Blood 81, no. 4 (February 15, 1993): 894–900. http://dx.doi.org/10.1182/blood.v81.4.894.bloodjournal814894.

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The effects of direct activators of protein kinase C (PKC) (the phorbol ester tetradecanoyl phorbol myristic acid [TPA] or bryostatin) on the ability of a highly enriched population of granulocyte-macrophage colony-forming cells (GM-CFC) to proliferate and develop in soft agar was assessed. In the absence of colony stimulating factors, the PKC activators did not stimulate colony formation. However, in the presence of optimal concentrations of granulocyte colony-stimulating factor (G- CSF) or interleukin-6 (IL-6), TPA or bryostatin markedly elevated the number of colonies formed from the GM-CFC. In the absence of TPA, IL-6, and G-CSF, respectively, both stimulated the formation of about 3% of the colonies observed when IL-3 was present. When TPA plus G-CSF or IL- 6 were added together, this figure increased to 48% and 54%, respectively. In both instances, the types of mature cells formed was altered from colonies of mature neutrophilic cells to a mixture consisting predominantly of macrophages with some neutrophils. Similar results were observed when bryostatin replaced TPA in these assays. When single cell colony-forming assays were performed, the same results were obtained. The presence of G-CSF, or IL-6, and the activator of PKC used (TPA or bryostatin) was required throughout the colony-forming assay for an optimal synergistic effect to be observed. These data indicate that agents that activate PKC can promote the proliferation and development of GM-CFC via a synergistic interaction with G-CSF or IL-6. Furthermore, there is an apparent role for PKC in development and possibly lineage commitment of GM-CFC.
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Chen, Chunhua, Junhua Tang, Shan Xu, Wenxia Zhang, and Hanliang Jiang. "miR-30a-5p Inhibits Proliferation and Migration of Lung Squamous Cell Carcinoma Cells by Targeting FOXD1." BioMed Research International 2020 (April 13, 2020): 1–14. http://dx.doi.org/10.1155/2020/2547902.

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Objective. To investigate the mechanism of miR-30a-5p inhibiting proliferation and migration of lung squamous cell carcinoma (LSCC) cells by targeting FOXD1. Methods. Bioinformatics was used to analyze differentially expressed genes in the TCGA_LUSC database. qRT-PCR was used to detect the expression levels of miR-30a-5p and FOXD1 in human normal lung epithelial cell line and human LSCC cell lines. The protein expression of FOXD1 was detected by western blot. The cell viability and colony formation abilities were examined by CCK-8 and colony formation assays, respectively. Wound healing and Transwell assays were performed to examine the migration and invasion abilities of cells. The targeted binding sites of miR-30a-5p and FOXD1 were predicted by bioinformatics, and dual luciferase assay was used to verify the targeted binding relationship between miR-30a-5p and FOXD1. Result. miR-30a-5p was downregulated in LSCC tissues and cells, while FOXD1 was highly expressed. Overexpression of miR-30a-5p or silencing FOXD1 inhibited cell viability, colony formation ability, migration, and invasion of LSCC cells. miR-30a-5p inhibited the proliferation and migration of LSCC cells by downregulating the expression of FOXD1. Conclusion. miR-30a-5p can downregulate the expression of FOXD1 and inhibit the proliferation and migration of LSCC.
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Han, Ruirui, Qianqian Sun, Jianbo Wu, Pengyuan Zheng, and Guoqiang Zhao. "Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells." Cellular Physiology and Biochemistry 39, no. 5 (2016): 1919–29. http://dx.doi.org/10.1159/000447889.

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Background: As the end product of the bacterial fermentation of dietary fiber in the colonic lumen, sodium butyrate (NaBt) has been reported to exert antitumor effects on colorectal cancer (CRC). In addition to functioning as a histone deacetylase (HDAC) inhibitor, NaBt also regulates the expression of microRNAs (miRNAs) to inhibit CRC cell proliferation. Yet, the mechanisms involved are not completely understood. Here we investigate whether NaBt regulates miR-203 to inhibit CRC growth and explore the promising target gene of miR-203 in CRC cells. Methods: We conducted qRT-PCR and Western blotting assays to evaluate the effects of NaBt on the expression of miR-203 and NEDD9 in HT-29 and Caco-2 cell lines. The promising target gene of miR-203 was predicted by miRNA target prediction and dual luciferase reporter assay. CRC Cell proliferation, colony formation, cell apoptosis and cell invasion assays were performed to explore the effect of NaBt, miR-203 and NEDD9 on HT-29 and Caco-2 cell lines. Results: The results showed that NaBt increased the expression of miR-203 to induce CRC cell apoptosis as well as inhibit cell proliferation, colony formation and cell invasion. Moreover, we determined that the NEDD9 was a target gene of miR-203. NEDD9 partially overcame the inhibitory effects of miR-203 on CRC cell colony formation and invasion. Conclusions: NaBt could induce CRC cell apoptosis, inhibit CRC cell proliferation, colony formation and invasion through miR-203/NEDD9 cascade. The present study may enrich the mechanisms underlying the process that NaBt exerts anti-tumor effects on CRC cells.
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Fan, Zhirui, Wenhua Xue, Mengmeng Dou, Lifeng Li, Jingli Lu, Bingjun Ma, Xiaoming Deng, et al. "Bushenshugan Formula Attenuates the Development of Lung Cancer by Inhibiting Epithelial-Mesenchymal Transition." Cellular Physiology and Biochemistry 47, no. 5 (2018): 1977–88. http://dx.doi.org/10.1159/000491466.

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Background/Aims: BushenShugan Formula (BSF) is a traditional Chinese medicine that has therapeutic effects on middle- and late-stage lung adenocarcinoma in clinical application. It was reported that Bushen Chinese medicine suppressed the onset of pre-metastatic niches in a murine model of spontaneous lung metastasis. However, the mechanisms of BSF on human lung adenocarcinoma remain unknown. Methods: Cell proliferation was determined by CCK8 and colony formation. Cell apoptosis and cell cycle were detected by flow cytometry. Cancer stem cells properties were examined by spheroid body formation. The migration and invasion abilities were analyzed by wound healing assay and transwell invasion assay. The mRNA expressions were determined by qRT-PCR. Western blotting analysis showed the protein levels. Results: BSF was shown to inhibit the proliferation of A549 cells in time- and concentration-dependent manners. Colony formation assays also indicated the antiproliferative effect of BSF against A549 cells. Cellular mechanistic studies demonstrated that BSF arrested the cell cycle in G2/M phase and induced apoptosis. Importantly, BSF could inhibit the epithelial-mesenchymal transition(EMT) of A549 cells through PI3K/AKT/NF-κB pathway. Conclusions: BSF effectively inhibited tumour growth, suggesting that it is a promising anticancer treatment for further clinical development.
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Linderholm, Angela L., Carrie L. Findleton, Gagandeep Kumar, Yeun Hong, and Linda F. Bisson. "Identification of Genes Affecting Hydrogen Sulfide Formation in Saccharomyces cerevisiae." Applied and Environmental Microbiology 74, no. 5 (January 11, 2008): 1418–27. http://dx.doi.org/10.1128/aem.01758-07.

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ABSTRACT A screen of the Saccharomyces cerevisiae deletion strain set was performed to identify genes affecting hydrogen sulfide (H2S) production. Mutants were screened using two assays: colony color on BiGGY agar, which detects the basal level of sulfite reductase activity, and production of H2S in a synthetic juice medium using lead acetate detection of free sulfide in the headspace. A total of 88 mutants produced darker colony colors than the parental strain, and 4 produced colonies significantly lighter in color. There was no correlation between the appearance of a dark colony color on BiGGY agar and H2S production in synthetic juice media. Sixteen null mutations were identified as leading to the production of increased levels of H2S in synthetic juice using the headspace analysis assay. All 16 mutants also produced H2S in actual juices. Five of these genes encode proteins involved in sulfur containing amino acid or precursor biosynthesis and are directly associated with the sulfate assimilation pathway. The remaining genes encode proteins involved in a variety of cellular activities, including cell membrane integrity, cell energy regulation and balance, or other metabolic functions. The levels of hydrogen sulfide production of each of the 16 strains varied in response to nutritional conditions. In most cases, creation of multiple deletions of the 16 mutations in the same strain did not lead to a further increase in H2S production, instead often resulting in decreased levels.
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Gordon, Jenna L., Melissa M. Reynolds, and Mark A. Brown. "Nitric Oxide as a Potential Adjuvant Therapeutic for Neuroblastoma: Effects of NO on Murine N2a Cells." Veterinary Sciences 7, no. 2 (April 23, 2020): 51. http://dx.doi.org/10.3390/vetsci7020051.

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Neuroblastoma, the most common extracranial solid tumor in children, accounts for 15% of all pediatric cancer deaths. Pharmaceutical applications of S-Nitrosylation, which, under normal conditions is involved with a host of epigenetic and embryological development pathways, have exhibited great potential for use as adjuvant therapeutics in the clinical management of cancer. Herein, an evaluation of the impact of nitric oxide (NO) as a potent anticancer agent on murine neuroblastoma cells is presented. Excitingly cell viability, colony formation, and non-carcinogenic cell analysis illustrate the significance and practicality of NO as a cytotoxic anticancer therapeutic. Resazurin, WST-8 (2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium, monosodium salt), and MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphyltetrazolium bromide) assays consistently displayed a moderate, ~20–25% reduction in cell viability after exposure to 1 mM S-Nitrosoglutathione (GSNO). A colony formation assay demonstrated that treated cells no longer exhibited colony formation capacity. Identically GSNO-treated Adult Human Dermal Fibroblasts (HDFa) exhibited no decrease in viability, indicating potential discrimination between neoplastic and normal cells. Collectively, our findings indicate a potential application for NO as an adjuvant therapeutic in the clinical management of neuroblastoma.
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Bashari, Muhammad Hasan, Saras Hidayat, Yasmin Anissa Robles Ruswandi, Tenny Putri, Nurul Qomarilla, Resti Gradia Dwiwina, Dikdik Kurnia, Mieke H. Satari, and Fathul Huda. "THE N-HEXANE FRACTION OF MYRMECODIA PENDANS INHIBITS CELL SURVIVAL AND PROLIFERATION IN COLON CANCER CELL LINE." International Journal of Pharmacy and Pharmaceutical Sciences 10, no. 1 (January 1, 2018): 108. http://dx.doi.org/10.22159/ijpps.2018v10i1.21882.

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Objective: Despite advanced treatment options available for colorectal cancer, many reported resistance and unresponsiveness to conventional chemotherapeutic agents. Therefore, it is urgent to discover a novel drug for colon cancer. Sarang Semut (Myrmecodia pendans), an Indonesian native plant, has been studied extensively due to its anti-cancer profiles. This study aimed to evaluate the anti-tumour activity of Sarang Semut in colon cancer cells.Methods: We evaluated cytotoxic activity of methanol extract as well as n-hexane and ethyl acetate fraction towards colon cancer cell lines (Caco-2 and HCT-116 cells) utilizing 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay. The most potent fraction was evaluated further in inhibiting cell survival using MTT assay and cell proliferation using trypan blue exclusion assay as well as a clonogenic assay.Results: Our data showed that the n-hexane fraction of Sarang Semut induces more cell death than the methanol extract and ethyl acetate fraction. Therefore, we analyzed the n-hexane fraction further and found that the inhibitory concentration 50% (IC50) of the n-hexane fraction was 24 and 30 parts per million (ppm) for Caco-2 and HCT-116 cells, respectively. Moreover, it inhibited cell growth as well as cell colony formation, in particular, shown by the plating efficiency (P<0.05) and colony area per seed (P<0.01) of the control group were different to the treatment group.Conclusion: The n-hexane fraction of Sarang Semut demonstrates a high potential antitumor activity in colon cancer cell line.
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Xu, Bo, Qin Shao, Kaipeng Xie, Yuqing Zhang, Tianyu Dong, Yankai Xia, and Wei Tang. "The Long Non-Coding RNA ENST00000537266 and ENST00000426615 Influence Papillary Thyroid Cancer Cell Proliferation and Motility." Cellular Physiology and Biochemistry 38, no. 1 (2016): 368–78. http://dx.doi.org/10.1159/000438637.

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Background/Aims: Papillary thyroid cancer (PTC) is the most common histotype of Thyroid cancer (TC). Here, we detected the differentially expressed lncRNAs in tumor tissues and non-tumor tissues of PTC patients by lncRNA microarrays, and explored the function and molecular mechanisms of lncRNAs in the pathogenesis of PTC using a PTC cell line. Methods: CCK-8 assay, colony formation assay and EdU assay were used to detect the cell viability. Flow Cytometry was used to detect the cell cycle and apoptosis. Transwell and scratch assay were used to detect the cell motility. Results: CCK-8 assay, colony formation assay and EdU assay revealed that lncRNAs (ENST00000537266 and ENST00000426615) could inhibit cell proliferation. Cell cycle analysis showed that cell proportion was statistically significant increased in G1 phase and decreased in S phase and G2 phase in Si-266 transfected TPC-1 cells. In addition, a noteworthy increase of cell proportion in G1 phase accompanied by a decrease in S phase and unchanged G2 phase in Si-615 transfected TPC-1 cells were also observed. Meanwhile, transwell and scratch assay showed that ENST00000426615 could inhibit the cell motility while ENST00000537266 could not. Conclusion: Our results showed that lncRNAs (ENST00000426615 and ENST00000537266) might be important regulators of PTC cell proliferation and motility, which might provide new insight into the understanding of PTC pathogenesis.
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Lv, Teng, Kejuan Song, Lili Zhang, Weihua Li, Yulong Chen, Yuchao Diao, Qin Yao, and Peishu Liu. "miRNA-34a decreases ovarian cancer cell proliferation and chemoresistance by targeting HDAC1." Biochemistry and Cell Biology 96, no. 5 (October 2018): 663–71. http://dx.doi.org/10.1139/bcb-2018-0031.

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Abstract:
This study aimed to explore the roles of miRNA-34a (miR-34a) in ovarian cancer (OC) cells and uncover possible mechanisms. The proliferation of OC cells was measured with an MTT assay and soft agar colony formation assay. TargetScan analysis, real-time PCR, and a luciferase reporter assay were used to demonstrate the downstream target of miR-34a in OC cells. HDAC1 expression levels were detected by immunoblot analysis. miR-34a inhibited the proliferation of SKOV3 and OVCA433 cells and enhanced cisplatin sensitivity in cisplatin-resistant SKOV3cp cells. The results of TargetScan analysis, real-time PCR, and luciferase reporter assay confirmed that miR-34a downregulated HDAC1 expression by directly targeting the 3′-UTR of HDAC1 mRNA. The overexpression of HDAC1 decreased cisplatin sensitivity and promoted proliferation in OC cells. MTT assay and soft agar colony formation assay showed that HDAC1 overexpression blocked the suppressive effects of miR-34a on SKOV3 cell proliferation. In addition, treatment with the miR-34a mimic partially recovered the cisplatin sensitivity of SKOV3cp cells, whereas HDAC1 overexpression blocked the above phenomena caused by treatment with the miR-34a mimic. miR-34a exhibited suppressive effects on OC cells via directly binding and downregulating HDAC1 expression, which subsequently decreased the resistance to cisplatin and suppressed proliferation in OC cells.
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50

Ema, H., T. Suda, Y. Miura, and H. Nakauchi. "Colony formation of clone-sorted human hematopoietic progenitors." Blood 75, no. 10 (May 15, 1990): 1941–46. http://dx.doi.org/10.1182/blood.v75.10.1941.1941.

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Abstract To characterize human hematopoietic progenitors, we performed methylcellulose cultures of single cells isolated from a population of CD34+ cells by fluorescence-activated cell-sorting (FACS) clone-sorting system. CD34+ cells were detected in bone marrow (BM) and peripheral blood (PB) cells at incidences of 1.0% and 0.01% of total mononuclear cells, respectively. Single cell cultures revealed that approximately 37% of BM CD34+ cells formed colonies in the presence of phytohemagglutinin-leukocyte conditioned medium and erythropoietin. Erythroid bursts-, granulocyte-macrophage (GM) colony-, and pure macrophage (Mac) colony-forming cells were 10% each in CD34+ cells. Approximately 15% of PB CD34+ cells formed colonies in which erythroid bursts were predominant. CD34+ cells were heterogeneous and fractionated by several antibodies in FACS multicolor analysis. In these fractionated cells, CD34+, CD33+ cells formed GM and Mac colonies 7 to 10 times as often as CD34+, CD33- cells. Most of the erythroid bursts and colonies were observed in the fraction of CD34+, CD13- cells or CD34+, CD33- cells. The expression of HLA-DR on CD34+ cells was not related to the incidence, size, or type of colonies. There was no difference in the phenotypical heterogeneity of CD34+ cells between BM and PB. About 10% of CD34+ cells were able to form G colonies in response to granulocyte colony-stimulating factor (G-CSF) and to form Mac colonies in GM-CSF or interleukin-3 (IL-3). Progenitors capable of generating colonies by stimulation of G-CSF were more enriched in CD34+, CD33+ fraction than in CD34+, CD33- fraction. Thus, single cell cultures using the FACS clone-sorting system provide an accurate estimation of hematopoietic progenitors and an assay system for direct action of colony-stimulating factors.
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