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Journal articles on the topic 'Malat 1'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Wang, Jun, Yongsheng Pan, Jie Wu, Cheng Zhang, Yuan Huang, Ruizhe Zhao, Gong Cheng, et al. "The Association between Abnormal Long Noncoding RNA MALAT-1 Expression and Cancer Lymph Node Metastasis: A Meta-Analysis." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1823482.

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Previous studies have investigated that the expression levels of MALAT-1 were higher in cancerous tissues than matched histologically normal tissues. And, to some extent, overexpression of MALAT-1 was inclined to lymph node metastasis. This meta-analysis collected all relevant articles and explored the association between MALAT-1 expression levels and lymph node metastasis. We searched PubMed, EmBase, Web of Science, Cochrane Library, and OVID to address the level of MALAT-1 expression in cancer cases and noncancerous controls (accessed February 2015). And 8 studies comprising 696 multiple cancer patients were included to assess this association. The odds ratio (OR) and its corresponding 95% confidence interval (CI) were calculated to assess the strength of the association using Stata 12.0 version software. The results revealed there was a significant difference in the incidence of lymph node metastasis between high MALAT-1 expression group and low MALAT-1 expression group (OR = 1.94, 95% CI 1.15–3.28, P=0.013 random-effects model). Subgroup analysis indicated that MALAT-1 high expression had an unfavorable impact on lymph node metastasis in Chinese patients (OR = 1.87, 95% CI 1.01–2.46). This study demonstrated that the incidence of lymph node metastasis in patients detected with high MALAT-1 expression was higher than that in patients with low MALAT-1 expression in China.

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Liu, Zhen-Feng, Qian-Ni Ye, Jun Yang, Min Yang, Dong-Hui Pan, and Meng-Jie Dong. "Preclinical evaluation of [68Ga]Ga-MALAT-1-antisense oligonucleotides for specific PET imaging of MALAT-1 expressing tumours." Nuclear Medicine Communications 42, no. 7 (March 1, 2021): 782–91. http://dx.doi.org/10.1097/mnm.0000000000001387.

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3

Balasis, Maria E., Jane Merelvede, Sateesh Kunigal, Xiaoyi Ren, Yan Ma, Qing Zhang, Jeff Painter, et al. "Molecular Characterization of SRSF2 Mutation Identifies a Clinically Relevant Lncrna (MALAT1) in Chronic Myelomonocytic Leukemia (CMML)." Blood 126, no. 23 (December 3, 2015): 1641. http://dx.doi.org/10.1182/blood.v126.23.1641.1641.

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Abstract SRSF2 is mutated at proline 95 (P95) in approximately 45% of patients with CMML. The consequence of SRSF2 P95H mutations on splicing has been associated with change in target RNA motif preference compared to wild type that favors CCNG over GGNG resulting in aberrant splicing abnormalities. Although this has led to several downstream mis-spliced candidates that may contribute to SRSF2 leukemic pathogenesis, the biologic consequences of SRSF2 mutation have not been fully elucidated and its effect on non-splicing pathways has yet to be explored. SRSF2 has two major functions within the nucleus: (1) bind to cis elements on pre-mRNA transcripts that functionally redefines putative exon-intron boundaries and (2) interact with other members of the spliceosome complex at nuclear suborganelles known as speckles. To explore the effects of SRSF2 P95 mutation on nuclear speckle dynamics, we transfected HeLa cells with GFP-SRSF2 wildtype (WT) and mutant (MT) constructs and performed Fluorescent Recovery After Photo-bleaching (FRAP) to determine the mutant specific kinetics of SRSF2 molecules localized to the nuclear speckle. Using this approach, we confirmed that SRSF2 WTs are characterized by complete photo-recovery with a half-life of approximately 35 (30-42) seconds as previously reported. However, when we performed FRAP of GFP-SRSF2 MTs a statistically significant difference in photo-recovery was observed compared to WT cells (Fig. 1a). The difference between baseline fluorescence and maximal recovered fluorescence in SRSF2 MT cells, or the immobile fraction, suggests that trapped bleached SRSF2 molecules are sterically inhibiting the diffusion of unbleached SRSF2 molecules. We reasoned that the observed differences in RNA binding capacity and nuclear speckle dynamics could be related. This rationale identified MALAT1 as a link connecting both increased RNA binding and nuclear speckle trafficking abnormalities because it is a Long Non-Coding (lnc) RNA that localizes to and has a critical role in SR protein recruitment and retention to the nuclear speckle. MALAT1, which is highly enriched for CCNG motifs, has also been demonstrated to bind to SRSF2 directly and has been implicated in a wide spectrum of carcinomas making it an attractive intermediary to study in our system. To determine whether SRSF2 MTs have increased MALAT1 binding capacity compared to SRSF2 WT, we performed RNA IP of myc-his-SRSF2 WT and MT transfected HeLa cells. Using this approach, we demonstrated a 60% enrichment of MALAT1 in SRSF2 WT transfected cells and a 120-150% enrichment of MALAT1 in SRSF2 MT cells compared to the empty vector control (Fig. 1b-c). We next performed the above FRAP experiment in the context of MALAT1 depletion and demonstrated that observed immobile fraction seen in SRSF2 MT cells is rescued (Fig. 1d). To determine the clinical relevance of MALAT1 in CMML we profiled a cohort of 54 CMML cases for MALAT1 expression by PCR. As shown in Figure 2a-b and d-e, MALAT1 expression is statistically elevated in CMML BMNCs and is among the highest differentially expressed transcripts in CMML monocytes (CD14+). We additionally characterized SRSF2 expression in our CMML BMNCs and CD14+ cohort and identified a linear correlation (Pearson R=0.7 p<0.05) between SRSF2 expression and MALAT1 expression (Figure 2c). Further, CMML patients with high MALAT1 expression in the BMNC compartment had inferior overall and leukemia-free survival (Fig. 2f-g). Given its relevance in solid tumors and its over-expression in CMML, we explored the consequence of MALAT1 depletion on human monocytic leukemic cells. We first performed ultra-deep RNA sequencing of the THP-1 cell line treated with two MALAT-1 depleting ASOs or matched chemistry specific controls. IPA analysis of differentially expressed transcripts identified a c-Myc gene signature that was validated by western blot analysis demonstrating reduction of c-Myc in THP-1 MALAT1-depleted cells. Colony formation assays using the THP-1 cell line demonstrated that MALAT-1 depletion resulted in decreased colony-forming capacity (CFC). MALAT-1 ASOs were also capable of depleting MALAT-1 in primary CMML BMNCs and were associated with a decreased CFC suggesting that MALAT-1 is a potential therapeutic target. Taken together, our data identifies SRSF2 P95 mutation nuclear trafficking abnormalities and identifies a novel clinically relevant lncRNA in CMML. Figure 1. Figure 1. Figure 2. Figure 2. Disclosures Komrokji: Celgene: Consultancy, Research Funding; Incite: Consultancy; Novartis: Speakers Bureau; GSK: Research Funding. List:Celgene Corporation: Honoraria, Research Funding.

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Alfaifi, Mohammed, Mirza Masroor Ali Beg, Mohammed Yahya Alshahrani, Irfan Ahmad, Ali Gaithan Alkhathami, Prakash C. Joshi, Osama M. Alshehri, Abdulrahman Manaa Alamri, and Amit Kumar Verma. "Circulating long non-coding RNAs NKILA, NEAT1, MALAT1, and MIAT expression and their association in type 2 diabetes mellitus." BMJ Open Diabetes Research & Care 9, no. 1 (January 2021): e001821. http://dx.doi.org/10.1136/bmjdrc-2020-001821.

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BackgroundType 2 diabetes mellitus (T2DM) is a multifactorial disorder that leads to alterations in gene regulation. Long non-coding RNAs (lncRNAs) have become a major research topic as they are involved in metabolic disorders.MethodsThis study included a total of 400 study subjects; 200 were subjects with T2DM and 200 were healthy subjects. Extracted RNA was used to synthesize cDNA by quantitative real time. Serum analysis was carried out to determine differences in biochemical parameters. Recorded data were used to evaluate associations with expression of lncRNAs NF-kappaB interacting lncRNA (NKILA), nuclear enriched abundant transcript 1 (NEAT1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), and myocardial infarction-associated transcript (MIAT) in T2DM cases.ResultsCompared with healthy controls, patients with T2DM showed an overall increase in expression of lncRNAs NKILA, NEAT, MALAT1, and MIAT by 3.94-fold, 5.28-fold, 4.46-fold, and 6.35-fold, respectively. Among patients with T2DM, higher expression of lncRNA NKILA was associated with hypertension (p=0.001), smoking (p<0.0001), and alcoholism (p<0.0001). Altered NEAT1 expression was significantly associated with weight loss (p=0.04), fatigue (p=0.01), slow wound healing (p=0.002), blurred vision (p=0.008), loss of appetite (p=0.007), smoking (p<0.0001), and alcoholism (p<0.0001). Higher expression of lncRNA MALAT1 was significantly linked with weight loss (p=0.003), blurred vision (p=0.01), smoking (p<0.0001), and alcoholism (p<0.0001). Expression of lncRNA MIAT was associated with only blurred vision (p<0.0001), smoking (p<0.0001), and alcoholism (p<0.0001). Positive correlations of lncRNA NKILA with lncRNAs NEAT1 (r=0.42, p<0.0001), MALAT (r=0.36, p<0.0001) and MIAT (r=0.42, p<0.0001) were observed among patients with T2DM. Significant positive correlations of lncRNA NEAT with lncRNAs MALAT and MIAT were observed among patients with T2DM. A positive correlation between lncRNAs MALAT and MIAT was also observed among patients with T2DM.ConclusionIncreased circulating NKILA, NEAT1, MALAT, and MIAT expression in patients with T2DM, which is linked with poor patient outcomes and significantly linked with alcoholism and smoking, may influence the degree and severity of disease among patients with T2DM. These lncRNAs may contribute to the progression of T2DM disease or other related diabetes-related complications.

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Fu, Shijian, Yanhong Wang, Hang Li, Leilei Chen, and Quanzhong Liu. "Regulatory Networks of LncRNA MALAT-1 in Cancer." Cancer Management and Research Volume 12 (October 2020): 10181–98. http://dx.doi.org/10.2147/cmar.s276022.

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6

Jos, B. "Ekstraksi Asam Tartrat Dan Asam Malat : Pengaruh Tri (6-Methyl) Amin Sebagai Extracting Power Dalam Berbagai Solven Terhadap Koefisien Distribusi." REAKTOR 9, no. 2 (June 19, 2017): 117. http://dx.doi.org/10.14710/reaktor.9.2.117-120.

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Limbah buangan industri minuman anggur masih mengandung asam tartrat dan asam malat. Dengan mereduksi kadar asam tartrat dan asam malat di dalam limbah akan mengurangi polusi yang ditimbulkan. Kemungkinan pengambilan kembali asam-asam ini dengan cara ekstraksi cair-cair telah berkembang. Dalam penelitian ini digunakan Tri (6-Methyl) Amin sebagai extracting power dalam berbagai solven seperti Hexanol-1; Chloroform, campuran Heptan (50%vol) + hexanol-1 (50%v); dan 2,6 DIMETHYL-4 Heptanon. Harga koefisien distribusi untuk masing-masing asam ditentukan berdasarkan konsentrasi amin dalam solven berkisar antara 0,1 sampai 0,8 mol amin per liter larutan. Koefisien distribusi asam tartrat yang diperoleh pada berbagai solven berkisar antara 2,5- 165,1; sedangakan untuk asam malat antara 1,7- 73,9. Dengan besarnya harga koefisien distribusi untuk masing-masing asam yang diperoleh Tri (6-Methyl) Amin sebagai extracting power dalam solven dapat digunakan untuk mengekstrak asam tartrat dan asam malat.Kata kunci : eksraksi cair-cair, asam tartrat, asam malat, amin

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7

Chen, Shaoan, Pengpeng Ma, Ying Zhao, Bin Li, Shaobo Jiang, Hui Xiong, Zheng Wang, Hanbo Wang, Xunbo Jin, and Chuan Liu. "Biological function and mechanism of MALAT-1 in renal cell carcinoma proliferation and apoptosis: role of the MALAT-1–Livin protein interaction." Journal of Physiological Sciences 67, no. 5 (September 21, 2016): 577–85. http://dx.doi.org/10.1007/s12576-016-0486-8.

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8

Yang, Feng, Fan Yi, Xiaorui Han, Quan Du, and Zicai Liang. "MALAT-1 interacts with hnRNP C in cell cycle regulation." FEBS Letters 587, no. 19 (August 20, 2013): 3175–81. http://dx.doi.org/10.1016/j.febslet.2013.07.048.

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9

Cheng, Yating, Parisa Imanirad, Indira Jutooru, Erik Hedrick, Un-Ho Jin, Aline Rodrigues Hoffman, Jeann Leal de Araujo, Benjamin Morpurgo, Andrei Golovko, and Stephen Safe. "Role of metastasis-associated lung adenocarcinoma transcript-1 (MALAT-1) in pancreatic cancer." PLOS ONE 13, no. 2 (February 1, 2018): e0192264. http://dx.doi.org/10.1371/journal.pone.0192264.

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10

Elamir, Azza M., Olfat G. Shaker, Mohamed HM El-Komy, Mai Mahmoud sharabi, and Nesreen M. Aboraia. "The role of LncRNA MALAT-1 and MiRNA-9 in Psoriasis." Biochemistry and Biophysics Reports 26 (July 2021): 101030. http://dx.doi.org/10.1016/j.bbrep.2021.101030.

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11

Yao, Jin, Xiao‐Qun Wang, Yu‐Jie Li, Kun Shan, Hong Yang, Yang‐Ning‐Zhi Wang, Mu‐Di Yao, et al. "Long non‐coding RNA MALAT 1 regulates retinal neurodegeneration through CREB signaling." EMBO Molecular Medicine 8, no. 4 (March 10, 2016): 346–62. http://dx.doi.org/10.15252/emmm.201505725.

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Yao, Jin, Xiao‐Qun Wang, Yu‐Jie Li, Kun Shan, Hong Yang, Yang‐Ning‐Zhi Wang, Mu‐Di Yao, et al. "Long non‐coding RNA MALAT 1 regulates retinal neurodegeneration through CREB signaling." EMBO Molecular Medicine 8, no. 9 (September 2016): 1113. http://dx.doi.org/10.15252/emmm.201606749.

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13

Tang, Ruixue, Mengtong Jiang, Lu Liang, Dandan Xiong, Yiwu Dang, and Gang Chen. "Long Noncoding RNA MALAT-1 Can Predict Poor Prognosis: A Meta-Analysis." Medical Science Monitor 22 (January 28, 2016): 302–9. http://dx.doi.org/10.12659/msm.895171.

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14

REN, DANYANG, HUIYING LI, RENQIU LI, JIANMING SUN, PIN GUO, HUIYUN HAN, YUEHUANG YANG, and JUN LI. "Novel insight into MALAT-1 in cancer: Therapeutic targets and clinical applications." Oncology Letters 11, no. 3 (January 22, 2016): 1621–30. http://dx.doi.org/10.3892/ol.2016.4138.

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15

Zhou, Yongqiang, Yun Li, Xiangnan Li, and Minjun Jiang. "Urinary Biomarker Panel to Improve Accuracy in Predicting Prostate Biopsy Result in Chinese Men with PSA 4–10 ng/mL." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/2512536.

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This study aims to evaluate the effectiveness and clinical performance of a panel of urinary biomarkers to diagnose prostate cancer (PCa) in Chinese men with PSA levels between 4 and 10 ng/mL. A total of 122 patients with PSA levels between 4 and 10 ng/mL who underwent consecutive prostate biopsy at three hospitals in China were recruited. First-catch urine samples were collected after an attentive prostate massage. Urinary mRNA levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The predictive accuracy of these biomarkers and prediction models was assessed by the area under the curve (AUC) of the receiver-operating characteristic (ROC) curve. The diagnostic accuracy of PCA3, PSGR, and MALAT-1 was superior to that of PSA. PCA3 performed best, with an AUC of 0.734 (95% CI: 0.641, 0.828) followed by MALAT-1 with an AUC of 0.727 (95% CI: 0.625, 0.829) and PSGR with an AUC of 0.666 (95% CI: 0.575, 0.749). The diagnostic panel with age, prostate volume, % fPSA, PCA3 score, PSGR score, and MALAT-1 score yielded an AUC of 0.857 (95% CI: 0.780, 0.933). At a threshold probability of 20%, 47.2% of unnecessary biopsies may be avoided whereas only 6.2% of PCa cases may be missed. This urinary panel may improve the current diagnostic modality in Chinese men with PSA levels between 4 and 10 ng/mL.

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Chen, Di, Lili Liu, Kai Wang, Haiyan Yu, Yafang Wang, Jiaming Liu, Yang Guo, and Hongbo Zhang. "The role of MALAT-1 in the invasion and metastasis of gastric cancer." Scandinavian Journal of Gastroenterology 52, no. 6-7 (March 1, 2017): 790–96. http://dx.doi.org/10.1080/00365521.2017.1280531.

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17

Wu, Mengli, Shuqiang Zhang, Xi Chen, Hui Xu, and Xiaoyu Li. "Expression and function of lncRNA MALAT-1 in the embryonic development of zebrafish." Gene 680 (January 2019): 65–71. http://dx.doi.org/10.1016/j.gene.2018.09.037.

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Liu, Chang, Xuesong Han, Bo Li, Shaobin Huang, Zhong Zhou, Zhiwei Wang, and Wanming Wang. "MALAT-1 is Associated with the Doxorubicin Resistance in U-2OS Osteosarcoma Cells." Cancer Management and Research Volume 13 (September 2021): 6879–89. http://dx.doi.org/10.2147/cmar.s304922.

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Alatas, Fikri, Fahmi Abdul Azizsidiq, Titta Hartyana Sutarna, Hestyari Ratih, and Sundani Nurono Soewandhi. "Perbaikan Kelarutan Albendazol Melalui Pembentukan Kristal Multikomponen dengan Asam Malat." Jurnal Farmasi Galenika (Galenika Journal of Pharmacy) (e-Journal) 6, no. 1 (March 7, 2020): 114–23. http://dx.doi.org/10.22487/j24428744.2020.v6.i1.14998.

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An effort to improve the solubility of albendazole (ABZ), an anthelmintic drug has been successfully carried out through the formation of multicomponent crystal with dl-malic acid (MAL). Construction of phase solubility curve of ABZ in MAL solution and crystal morphological observations after recrystallization in the acetone-ethanol (9:1) mixture were performed for initial prediction of multicomponent crystal formation. ABZ-MAL multicomponent crystal was prepared by wet grinding or also known as solvent-drop grinding (SDG) with acetone-ethanol (9:1) mixture as a solvent followed by characterization of the multicomponent crystal formation by powder X-ray diffraction and Fourier transform infrared (FTIR) methods. The solubility of ABZ-MAL multicomponent crystal was tested in water at ambient temperature and in pH 1.2, 4.5 and 6.8 of buffered solutions at 37°C. The phase solubility curve of the ABZ in the MAL solution showed type Bs. The ABZ-MAL mixture has a different crystalline morphology than pure ABZ and MAL after recrystallization in the acetone-ethanol mixture (9:1). The powder X-ray diffraction pattern and the FTIR spectrum of ABZ-MAL from SDG different from intact ABZ and MAL powder X-ray diffraction patterns and these results can indicate the ABZ-MAL multicomponent crystal formation. The ABZ-MAL multicomponent crystal has better solubility than pure ABZ in all media used. These results can be concluded that ABZ-MAL multicomponent crystal can be prepared by solvent-drop grinding method with acetone-ethanol (9:1) mixture as a solvent and can increase the solubility of albendazole.

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Jiao, Feng, Hai Hu, Ting Han, Cuncun Yuan, Lei Wang, Ziliang Jin, Zhen Guo, and Liwei Wang. "Long Noncoding RNA MALAT-1 Enhances Stem Cell-Like Phenotypes in Pancreatic Cancer Cells." International Journal of Molecular Sciences 16, no. 12 (March 24, 2015): 6677–93. http://dx.doi.org/10.3390/ijms16046677.

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21

Lee, Sang Kil, Jung Hwa Lee, Na Keum Lee, and Chan Hyuk Park. "Sa1983 Long Non-Coding RNA MALAT-1 Promote Invasion and Migration of Gastric Cancer." Gastroenterology 148, no. 4 (April 2015): S—374. http://dx.doi.org/10.1016/s0016-5085(15)31256-7.

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Li, Xiujun, Jiali Wang, Yuchen Pan, Yujun Xu, Dan Liu, Yayi Hou, and Guangfeng Zhao. "Long non-coding RNA HULC affects the proliferation, apoptosis, migration, and invasion of mesenchymal stem cells." Experimental Biology and Medicine 243, no. 13 (September 2018): 1074–82. http://dx.doi.org/10.1177/1535370218804781.

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Further studies on the molecular mechanisms of mesenchymal stem cells in the maintenance of growth and function are essential for their clinical application. Growing evidence has shown that long non-coding RNAs (lncRNAs) play an important role in the regulation of mesenchymal stem cells. Recently, it is reported that highly upregulated in liver cancer (HULC), with another lncRNA MALAT-1, accelerated liver cancer stem cell growth. The regulating role of MALAT-1 in mesenchymal stem cells has been investigated. However, the effects of HULC on the mesenchymal stem cells are unknown. In this study, we overexpressed HULC in mesenchymal stem cells derived from umbilical cord and analyzed the cell phenotypes, proliferation, apoptosis, migration, invasion and differentiation of mesenchymal stem cells. We found that overexpression of HULC significantly promotes cell proliferation through promoting cell division and inhibits cell apoptosis. HULC-overexpressed mesenchymal stem cells migrate and invade faster than control mesenchymal stem cells. HULC has no effect on phenotypes and differentiation of mesenchymal stem cells. Furthermore, we found that the expression of HULC in mesenchymal stem cells could be reduced by several inflammatory factors, including TNF-α, TGF-β1, and R848. Taken together, our data demonstrated that HULC has a vital role in the growth and function maintenance of mesenchymal stem cells without affecting differentiation. Impact statement Exploring the molecular mechanisms of growth and function in MSCs is the key to improve their clinical therapeutic effects. Currently, more and more evidence show that the long non-coding RNA (lncRNA) plays an important role in the growth, stemness and function of MSCs.Both HULC and MALAT1 are the earliest discovered LNCRNAs, which are closely related to tumor growth. All of them can promote the growth of liver cancer stem cells. Previously, we have studied the effects of MALAT1 on the growth and function of MSCs. In this study, we focused on the effects of HULC on MSCs. We elucidated the effects of HULC on the growth and differentiation of MSCs, and explored the relationship between inflammatory stimuli and HULC expression in MSCs. Our findings provide a new molecular target for the growth and clinical application of MSCs.

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23

Yang, Huaxia, Naixin Liang, Min Wang, Yunyun Fei, Jian Sun, Zhiyuan Li, Yuan Xu, et al. "Long noncoding RNA MALAT-1 is a novel inflammatory regulator in human systemic lupus erythematosus." Oncotarget 8, no. 44 (August 24, 2017): 77400–77406. http://dx.doi.org/10.18632/oncotarget.20490.

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Barsoum, Farida S., Amany S. Awad, Nada H. Hussein, Reda A. Eissa, and Hend M. El Tayebi. "MALAT-1: LncRNA ruling miR-182/PIG-C/mesothelin triad in triple negative breast cancer." Pathology - Research and Practice 216, no. 12 (December 2020): 153274. http://dx.doi.org/10.1016/j.prp.2020.153274.

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Puthanveetil, Prasanth, Shali Chen, Biao Feng, Anirudh Gautam, and Subrata Chakrabarti. "Long non‐coding RNA MALAT 1 regulates hyperglycaemia induced inflammatory process in the endothelial cells." Journal of Cellular and Molecular Medicine 19, no. 6 (March 19, 2015): 1418–25. http://dx.doi.org/10.1111/jcmm.12576.

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Ying, Liang, Qi Chen, Yawei Wang, Zhihua Zhou, Yiran Huang, and Feng Qiu. "Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition." Molecular BioSystems 8, no. 9 (2012): 2289. http://dx.doi.org/10.1039/c2mb25070e.

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Zhu, Lucheng, Jihong Liu, Shenglin MA, and Shirong Zhang. "Long Noncoding RNA MALAT-1 Can Predict Metastasis and a Poor Prognosis: a Meta-Analysis." Pathology & Oncology Research 21, no. 4 (July 10, 2015): 1259–64. http://dx.doi.org/10.1007/s12253-015-9960-5.

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Volkohon, A. D., V. Yu Harbuzova, and O. V. Ataman. "rs3200401 MALAT1 GENE POLYMORPHISM IS NOT RELATED TO AGE OF KIDNEY CANCER ONSET." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 2 (July 6, 2020): 119–23. http://dx.doi.org/10.31718/2077-1096.20.2.119.

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Today, the long non-coding RNA MALAT1 is considered to be one of the major RNAs involved in the emergence and metastasizing of various malignant tumours. Recent experiments have shown that MALAT1 plays an important role in the onset and progression of kidney cancer as well. It was found that cancer patient survival depends on the level of MALAT1 gene expression. The aim of the study was to investigate the possible association between rs3200401 MALAT1 gene polymorphism and age of kidney cancer onset among Ukrainian patients. Materials and methods. The venous blood of 101 patients with clear cell renal cell carcinoma (42 women and 59 men) was used for study. Determination of MALAT1 gene rs320040 polymorphism was performed by the Real-Time polymerase chain reaction method using TaqManSNP Assay C_3246069_10 components. Statistical analysis of the data obtained was performed using SPSS (version 17.0). To test the possible association between rs3200401 genotypes and the age of kidney cancer onset Kaplan-Meier and Cox regression techniques were used. P value < 0.05 was considered as statistically significant. Results. The obtained results of MALAT1 gene rs3200401 polymorphic site genotyping revealed that 71 (70.3%) patients with renal cell carcinoma had CC genotype, 29 (28.7%) – CT, 1 (1%) – TT genotype. Survival analysis by Kaplan-Meier method showed that life expectancy until the tumour occurrence was not related to rs3200401 locus (log rank P = 0.449 – for codominant model; log rank P = 0.847 – for dominant model). The results of Cox regression analysis also showed no link between MALAT gene rs3200401-site and risk of renal cell carcinoma development (P > 0.05). No statistically significant results were found after adjustment for sex, body mass index, metastasis, smoking and drinking habits (P > 0.05). Conclusions. The rs3200401 gene polymorphism of long non-coding RNA MALAT1 is not associated with the age of kidney cancer onset in Ukrainian population.

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Chen, Yan, Zhenzhou Xiao, Minhua Hu, Xiaoli Luo, and Zhaolei Cui. "Diagnostic efficacy of long non-coding RNA MALAT-1 in human cancers: a meta-analysis study." Oncotarget 8, no. 60 (September 18, 2017): 102291–300. http://dx.doi.org/10.18632/oncotarget.21013.

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Ren, Shancheng, Yawei Liu, Weidong Xu, Yi Sun, Ji Lu, Fubo Wang, Min Wei, et al. "Long Noncoding RNA MALAT-1 is a New Potential Therapeutic Target for Castration Resistant Prostate Cancer." Journal of Urology 190, no. 6 (December 2013): 2278–87. http://dx.doi.org/10.1016/j.juro.2013.07.001.

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Yang, Lin, Fei Xu, Miao Zhang, Xiao-Ying Shang, Xin Xie, Tao Fu, Jian-Ping Li, and Hong-Lin Li. "Role of LncRNA MALAT-1 in hypoxia-induced PC12 cell injury via regulating p38MAPK signaling pathway." Neuroscience Letters 670 (March 2018): 41–47. http://dx.doi.org/10.1016/j.neulet.2018.01.036.

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Tian, Yongjing, Xiuying Zhang, Yinghua Hao, Zhengyu Fang, and Yanling He. "Potential roles of abnormally expressed long noncoding RNA UCA1 and Malat-1 in metastasis of melanoma." Melanoma Research 24, no. 4 (August 2014): 335–41. http://dx.doi.org/10.1097/cmr.0000000000000080.

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Kulkarni, Priyanka, Pritha Dasgupta, Nadeem S. Bhat, Varahram Shahryari, Marisa Shiina, Yutaka Hashimoto, Shahana Majid, et al. "Elevated miR-182-5p Associates with Renal Cancer Cell Mitotic Arrest through Diminished MALAT-1 Expression." Molecular Cancer Research 16, no. 11 (July 23, 2018): 1750–60. http://dx.doi.org/10.1158/1541-7786.mcr-17-0762.

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Gutschner, Tony, Moritz Eißmann, Monika Hämmerle, Marion Stentrup, Catherina Hildenbrandt, Matthias Groß, Martin Zörnig, and Sven Diederichs. "Abstract A21: MALAT-1 is essential for lung cancer metastasis in a novel human knockout model." Cancer Research 72, no. 2 Supplement (January 8, 2012): A21. http://dx.doi.org/10.1158/1538-7445.nonrna12-a21.

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Zhao, Ziyi, Changjin Chen, Yu Liu, and Chuanfang Wu. "17β-Estradiol treatment inhibits breast cell proliferation, migration and invasion by decreasing MALAT-1 RNA level." Biochemical and Biophysical Research Communications 445, no. 2 (March 2014): 388–93. http://dx.doi.org/10.1016/j.bbrc.2014.02.006.

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Samir, A., F. Barsoum, R. E. Abdeltawab, and H. M. El Tayebi. "132P MALAT-1 ruling the miR-182/PIG-C/MSLN triad in triple negative breast cancer." Annals of Oncology 31 (May 2020): S59—S60. http://dx.doi.org/10.1016/j.annonc.2020.03.234.

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Lai, Ming-chun, Zhe Yang, Lin Zhou, Qian-qian Zhu, Hai-yang Xie, Feng Zhang, Li-ming Wu, Lei-ming Chen, and Shu-sen Zheng. "Long non-coding RNA MALAT-1 overexpression predicts tumor recurrence of hepatocellular carcinoma after liver transplantation." Medical Oncology 29, no. 3 (June 16, 2011): 1810–16. http://dx.doi.org/10.1007/s12032-011-0004-z.

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Xiao, Yiwen, Jingjing Pan, Qian Geng, and Ge Wang. "Lnc RNA MALAT 1 increases the stemness of gastric cancer cells via enhancing SOX 2 mRNA stability." FEBS Open Bio 9, no. 7 (June 2, 2019): 1212–22. http://dx.doi.org/10.1002/2211-5463.12649.

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Hong, C., S. Lin, and C. Lee. "151 CCL21 induces mTOR-dependent malat-1 expression, leading to cell migration in cutaneous T cell lymphoma." Journal of Investigative Dermatology 138, no. 5 (May 2018): S26. http://dx.doi.org/10.1016/j.jid.2018.03.156.

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Tano, Keiko, Rie Mizuno, Tomoko Okada, Randeep Rakwal, Junko Shibato, Yoshinori Masuo, Kenichi Ijiri, and Nobuyoshi Akimitsu. "MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes." FEBS Letters 584, no. 22 (October 10, 2010): 4575–80. http://dx.doi.org/10.1016/j.febslet.2010.10.008.

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Khater, N., D. Habashy, R. A. Youness, and M. Z. Gad. "14P MALAT-1: A novel LncRNA modulating STAT-3 regulated cystathionine-γ-lyase (CSE) in breast cancer." Annals of Oncology 32 (March 2021): S7. http://dx.doi.org/10.1016/j.annonc.2021.01.027.

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Mesaeli, Nasrin. "Role of calreticulin in the regulation of long non-coding RNA: MALAT-1 expression in mouse adenocarcinoma cells." Qatar Foundation Annual Research Forum Proceedings, no. 2013 (November 2013): BIOP 0132. http://dx.doi.org/10.5339/qfarf.2013.biop-0132.

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Hu, Qiongying, Shuiqin Li, Changjin Chen, Menglin Zhu, Yiming Chen, and Ziyi Zhao. "17β-Estradiol treatment drives Sp1 to upregulate MALAT-1 expression and epigenetically affects physiological processes in U2OS cells." Molecular Medicine Reports 15, no. 3 (January 12, 2017): 1335–42. http://dx.doi.org/10.3892/mmr.2017.6115.

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JIAO, FENG, HAI HU, CUNCUN YUAN, LEI WANG, WEIHUA JIANG, ZILIANG JIN, ZHEN GUO, and LIWEI WANG. "Elevated expression level of long noncoding RNA MALAT-1 facilitates cell growth, migration and invasion in pancreatic cancer." Oncology Reports 32, no. 6 (September 26, 2014): 2485–92. http://dx.doi.org/10.3892/or.2014.3518.

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Peters, Tim, Steffie Hermans-Beijnsberger, Abdelaziz Beqqali, Nicole Bitsch, Shinichi Nakagawa, Kannanganattu V. Prasanth, Leon J. de Windt, Ralph J. van Oort, Stephane Heymans, and Blanche Schroen. "Long Non-Coding RNA Malat-1 Is Dispensable during Pressure Overload-Induced Cardiac Remodeling and Failure in Mice." PLOS ONE 11, no. 2 (February 26, 2016): e0150236. http://dx.doi.org/10.1371/journal.pone.0150236.

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Wu, Jiasheng, Yueyue Weng, Fei He, Dong Liang, and Lin Cai. "LncRNA MALAT-1 competitively regulates miR-124 to promote EMT and development of non-small-cell lung cancer." Anti-Cancer Drugs 29, no. 7 (August 2018): 628–36. http://dx.doi.org/10.1097/cad.0000000000000626.

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Zhou, Yanqing, Xiaying Xu, Huabing Lv, Qirong Wen, Juan Li, Linyu Tan, Jianqi Li, and Xiujie Sheng. "The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration." PLOS ONE 11, no. 5 (May 26, 2016): e0155250. http://dx.doi.org/10.1371/journal.pone.0155250.

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Gao, Da, Ai-e. Lv, Hui-Ping Li, Dong-Hai Han, and Ya-Peng Zhang. "LncRNA MALAT-1 Elevates HMGB1 to Promote Autophagy Resulting in Inhibition of Tumor Cell Apoptosis in Multiple Myeloma." Journal of Cellular Biochemistry 118, no. 10 (May 3, 2017): 3341–48. http://dx.doi.org/10.1002/jcb.25987.

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Miyagawa, R., K. Tano, R. Mizuno, Y. Nakamura, K. Ijiri, R. Rakwal, J. Shibato, et al. "Identification of cis- and trans-acting factors involved in the localization of MALAT-1 noncoding RNA to nuclear speckles." RNA 18, no. 4 (February 21, 2012): 738–51. http://dx.doi.org/10.1261/rna.028639.111.

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Kryger, Rosemarie, Li Fan, Peter A. Wilce, and Vincent Jaquet. "MALAT-1, a non protein-coding RNA is upregulated in the cerebellum, hippocampus and brain stem of human alcoholics." Alcohol 46, no. 7 (November 2012): 629–34. http://dx.doi.org/10.1016/j.alcohol.2012.04.002.

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