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Journal articles on the topic 'TAM, miR-155, tumor microenvironment'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Szebeni, Gabor J., Csaba Vizler, Klara Kitajka, and Laszlo G. Puskas. "Inflammation and Cancer: Extra- and Intracellular Determinants of Tumor-Associated Macrophages as Tumor Promoters." Mediators of Inflammation 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/9294018.

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One of the hallmarks of cancer-related inflammation is the recruitment of monocyte-macrophage lineage cells to the tumor microenvironment. These tumor infiltrating myeloid cells are educated by the tumor milieu, rich in cancer cells and stroma components, to exert functions such as promotion of tumor growth, immunosuppression, angiogenesis, and cancer cell dissemination. Our review highlights the ontogenetic diversity of tumor-associated macrophages (TAMs) and describes their main phenotypic markers. We cover fundamental molecular players in the tumor microenvironment including extra- (CCL2, C

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2

Husain, Kazim, Krystal Villalobos-Ayala, Valentina Laverde, et al. "Apigenin Targets MicroRNA-155, Enhances SHIP-1 Expression, and Augments Anti-Tumor Responses in Pancreatic Cancer." Cancers 14, no. 15 (2022): 3613. http://dx.doi.org/10.3390/cancers14153613.

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Pancreatic cancer (PC) is a deadly disease with a grim prognosis. Pancreatic tumor derived factors (TDF) contribute to the induction of an immunosuppressive tumor microenvironment (TME) that impedes the effectiveness of immunotherapy. PC-induced microRNA-155 (miRNA-155) represses expression of Src homology 2 (SH2) domain-containing Inositol 5′-phosphatase-1 (SHIP-1), a regulator of myeloid cell development and function, thus impacting anti-tumor immunity. We recently reported that the bioflavonoid apigenin (API) increased SHIP-1 expression which correlated with the expansion of tumoricidal mac

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3

Gerloff, Dennis, Jana Lützkendorf, Rose K. C. Moritz, et al. "Melanoma-Derived Exosomal miR-125b-5p Educates Tumor Associated Macrophages (TAMs) by Targeting Lysosomal Acid Lipase A (LIPA)." Cancers 12, no. 2 (2020): 464. http://dx.doi.org/10.3390/cancers12020464.

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Tumor-associated macrophages (TAMs) are the most abundant immune cells in the tumor microenvironment, promoting tumor initiation, growth, progression, metastasis, and immune evasion. Recently it was shown that cancer cell-derived exosomes induce a tumor-promoting phenotype in TAMs. Exosome-loaded proteins, DNA, and RNAs may contribute to the macrophage reprogramming. However, the exact mediators and mechanisms, particularly in melanoma, are not known. In this study we examined the effects of cutaneous melanoma-derived exosomes on macrophage function and the underlying mechanisms. First, we sho

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Gajeton, Jasmine, Irene Krukovets, Santoshi Muppala, Dmitriy Verbovetskiy, Jessica Zhang, and Olga Stenina-Adognravi. "Hyperglycemia-Induced miR-467 Drives Tumor Inflammation and Growth in Breast Cancer." Cancers 13, no. 6 (2021): 1346. http://dx.doi.org/10.3390/cancers13061346.

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The tumor microenvironment contains the parenchyma, blood vessels, and infiltrating immune cells, including tumor-associated macrophages (TAMs). TAMs affect the developing tumor and drive cancer inflammation. We used mouse models of hyperglycemia and cancer and specimens from hyperglycemic breast cancer (BC) patients to demonstrate that miR-467 mediates the effects of high blood glucose on cancer inflammation and growth. Hyperglycemic patients have a higher risk of developing breast cancer. We have identified a novel miRNA-dependent pathway activated by hyperglycemia that promotes BC angiogene

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Murugan, Poongkavithai Vadevoo Sri, Gunassekaran Gowri Rangaswamy, and Byungheon Lee. "Abstract 2870: Inhibition of DNA methylation and histone deacetylation synergistically reprograms M2-polarized macrophages and inhibits tumor growth by upregulating miR-7083-5p." Cancer Research 83, no. 7_Supplement (2023): 2870. http://dx.doi.org/10.1158/1538-7445.am2023-2870.

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Abstract Reactivation of epigenetically suppressed miRs, in tumors, have become increasingly relevant in clinical practice. But less epigenetic studies have been performed on tumor associated M2 macrophages that plays a key role in the functional regulation of epithelial cancer development. In this study, we used 5-Aza-2’5’Aza-deoxycytidine (Aza) or decitabine (5-Aza) plus Trichostatin A (TSA) as epigenetic drugs to study the M2 macrophage modulation in the tumor microenvironment. Epigenetic therapy, not only modulated the M2 macrophages to a tumoricidal phenotype, but also strengthened the tu

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Arora, Shweta, Prithvi Singh, Shaniya Ahmad, et al. "Comprehensive Integrative Analysis Reveals the Association of KLF4 with Macrophage Infiltration and Polarization in Lung Cancer Microenvironment." Cells 10, no. 8 (2021): 2091. http://dx.doi.org/10.3390/cells10082091.

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Macrophage polarization and infiltration to the tumor microenvironment (TME) is a critical determining factor for tumor progression. Macrophages are polarized into two states—M1 (pro-inflammatory, anti-tumorigenic and stimulated by LPS or IFN-γ) and M2 (anti-inflammatory pro-tumorigenic and stimulated by IL-4) phenotypes. Specifically, M2 macrophages enhance tumor cell growth and survival. Recent evidences suggest the pivotal role of microRNAs in macrophage polarization during the development of Non-small cell lung cancer (NSCLC), thus proposing a new therapeutic option to target lung cancer.

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7

Banerjee, Hirendra, Christopher Krauss, Myla Worthington, et al. "Differential expression of efferocytosis and phagocytosis associated genes in tumor associated macrophages exposed to African American patient derived prostate cancer microenvironment." Journal of Solid Tumors 9, no. 2 (2019): 22. http://dx.doi.org/10.5430/jst.v9n2p22.

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Macrophages are the first line of defense in the cellular environment in response to any antigenic or foreign invasion. Since cancer cells express antigenic molecules and create a tumor microenvironment quite different from the normal cellular environment, macrophages will attack this cancer cells as foreign Invaders. However, the cancer cells adept their ability to suppress macrophage activity by secreting compounds/proteins through unknown mechanisms and train these macrophages to aid in tumorigenesis. These macrophages are commonly known as tumor associated macrophages (TAM). In this study,

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8

Chen, Hao, Chao Tang, Chun Tan, et al. "IL-2 Modulates TAMs Derived Exosomal MiRNAs to Ameliorate Hepatocellular Carcinoma Development and Progression." Journal of Oncology 2022 (February 21, 2022): 1–11. http://dx.doi.org/10.1155/2022/3445350.

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Background. Interleukin-2 (IL-2) is proved to play an irreplaceable role in antitumor regulation in numerous experimental and clinical trials. Tumor-associated macrophages (TAMs) are able to release exosomes to promote the development and progression of hepatocellular carcinoma (HCC) as essential component of microenvironment. In this study, our intention is to explore the effects of the exosomes from TAMs with IL-2 treatment on HCC development. TAMs were collected and cultured from HCC tissues. The exosomes from the TAMs treated with IL-2 (ExoIL2-TAM) or not (ExoTAM) were identified and used

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9

Yu, Haiyang, Jing Pan, Siyue Zheng, et al. "Hepatocellular Carcinoma Cell-Derived Exosomal miR-21-5p Induces Macrophage M2 Polarization by Targeting RhoB." International Journal of Molecular Sciences 24, no. 5 (2023): 4593. http://dx.doi.org/10.3390/ijms24054593.

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M2-like polarized tumor-associated macrophages (TAMs) are the major component of infiltrating immune cells in hepatocellular carcinoma (HCC), which have been proved to exhibit significant immunosuppressive and pro-tumoral effects. However, the underlying mechanism of the tumor microenvironment (TME) educating TAMs to express M2-like phenotypes is still not fully understood. Here, we report that HCC-derived exosomes are involved in intercellular communications and exhibit a greater capacity to mediate TAMs’ phenotypic differentiation. In our study, HCC cell-derived exosomes were collected and u

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Zelli, Veronica, Alessandra Corrente, Chiara Compagnoni, et al. "Ultrasound as a New Method for the Release and Identification of Novel microRNAs and Proteins as Candidate Biomarkers in Pancreatic Cancer." Cancers 17, no. 12 (2025): 1979. https://doi.org/10.3390/cancers17121979.

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Background/Objectives: Pancreatic cancer (PC) is among the most aggressive malignancies, often diagnosed at late stages. MicroRNAs (miRNAs) and proteins released from the tumor microenvironment into body fluids represent promising non-invasive biomarkers for early cancer detection. In this study, we took advantage of an innovative ultrasound (US)-based instrument (SonoWell®, Inno-Sol srl, Rome, Italy) to treat PC cells in order to promote and amplify the release of molecules, with the aim of identifying novel putative diagnostic PC biomarkers. Methods: Three human pancreatic adenocarcinoma cel

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Toldo, Nicolo, Verena Martinez Rodriguez, and Muller Fabbri. "Abstract LB297: Toll-like receptor 8 in tumor associated macrophages regulates miR-192-5p expression and drug resistance in neuroblastoma." Cancer Research 84, no. 7_Supplement (2024): LB297. http://dx.doi.org/10.1158/1538-7445.am2024-lb297.

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Abstract MicroRNAs (miRs) are small non-coding RNAs (ncRNAs) with gene expression regulatory functions. MiRs are frequently dys-regulated in human cancers and orchestrate the biology of the disease, and its resistance to chemotherapy. Increasing evidence supports a role of the tumor microenvironment (TME) in promoting cancer growth and resistance to treatments. Tumor Associated Macrophages (TAMs) are a predominant cellular component of the TME of several types of cancers, including neuroblastoma (NB), the most frequent pediatric extra-cranial solid tumor. NB cells secrete miRs within small ext

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Chang, Q., and Y. Liu. "JS03.6.A TUMOR ASSOCIATED MACROPHAGE DERIVED EXOSOMES MODULATE IMMUNOTHERAPEUTIC SENSITIVITY OF SHH MEDULLOBLASTOMA BY TARGETING M6A MODIFIED FOXD1." Neuro-Oncology 26, Supplement_5 (2024): v10. http://dx.doi.org/10.1093/neuonc/noae144.025.

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Abstract BACKGROUND Medulloblastoma (MB) is the most common malignant brain tumor in children. The infiltration of tumor-associated macrophages (TAMs) in tumor microenvironment (TME) is correlated with the poor prognosis in SHH subtype of MB patients. Epigenetic alterations on RNA m6A modification were identified in this tumor. However, it remains unclear whether the TAMs infiltration in TME was correlated with the m6A modification status during tumor progression. METHODS The expression of m6A modification-related proteins and TAMs specific marker were assessed by immunohistochemistry in 40 SH

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Miura, Yuji, Takanobu Motoshima, Nanako Wakigami, et al. "Phenotypic differences in tumor-associated macrophages between metastatic and primary sites of clear cell renal cell carcinoma." Journal of Clinical Oncology 36, no. 5_suppl (2018): 105. http://dx.doi.org/10.1200/jco.2018.36.5_suppl.105.

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105 Background: Tumor-associated macrophages (TAMs) are one of the key contributors to the tumor microenvironment and are phenotypically differentiated into M1 and M2 macrophages. M1 macrophages stimulate anti-tumor immune responses, whereas M2 macrophages promote immunosuppression and are associated with tumor progression in clear cell renal cell carcinoma (ccRCC). However, little information is available regarding the difference in TAM polarization between primary and metastatic lesions of ccRCC. Methods: We collected paired samples of primary and matched metastatic sites from the first recu

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Feng, Zhengzhe, Xiaoxi Zhang, Li Li, et al. "Tumor-associated macrophage-derived exosomal microRNA-155-5p stimulates intracranial aneurysm formation and macrophage infiltration." Clinical Science 133, no. 22 (2019): 2265–82. http://dx.doi.org/10.1042/cs20190680.

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Abstract Tumor-associated macrophages (TAMs) play a regulatory role in inflammation and cancer. Exosomes derived from macrophages carrying microRNAs (miRNAs or miRs) are of great value for cancer therapy. Gremlin 1 (GREM1), a member of the antagonists of secreted bone morphogenetic protein, has been implicated in the pathophysiology of multiple diseases or cancers. Based on the predictions of miRNA–mRNA interaction, GREM1 was found to be a target gene of miR-155-5p. Here, the present study aims to explore the role of TAM-derived exosomal miR-155-5p by regulating GREM1 in intracranial aneurysm

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Huffaker, Thomas, and Ryan O’Connell. "Single cell sequencing reveals regulatory role for T cell expressed microRNA-155 within the tumor microenvironment." Journal of Immunology 200, no. 1_Supplement (2018): 178.4. http://dx.doi.org/10.4049/jimmunol.200.supp.178.4.

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Abstract MicroRNA-155 (miR-155) is a pro-inflammatory miRNA that has been shown to regulate antitumor immunity. We recently demonstrated, utilizing miR-155 T cell conditional knockout mice (TCKO), that miR-155 is required by T cells to inhibit the growth of transplanted B16f10 melanoma tumors. To further understand the role of miR-155 expression within tumor infiltrating T cells and their impact upon the tumor microenvironment, we performed 10× single cell RNA-sequencing on tumor infiltrating immune cells from miR-155 TCKO mice and controls. At 12 days post administration of B16f10 OVA syngene

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Fan, Daping, and Junfeng Wang. "microRNA-155 is a master regulator of dendritic cell function in breast cancer." Journal of Immunology 196, no. 1_Supplement (2016): 75.12. http://dx.doi.org/10.4049/jimmunol.196.supp.75.12.

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Abstract In anti-tumor immunity, dendritic cells (DCs) capture, process and present tumor antigens to T cells, and initiate a tumoricidal response. However, DCs are often found dysfunctional due to their exposure to the tumor microenvironment (TME), leading to tumor escape from immune surveillance. The mechanisms underlying the regulation or dysregulation of DC function in the context of tumor has not been well elucidated. Here a vital role of microRNA-155 (miR-155) in regulating the function of DCs in breast cancer is reported. miR-155 expression is closely correlated with the maturation stat

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Chen, Guidong, and Jinpu Yu. "Abstract 6589: Exosomal miR-155-5p from early myeloid-derived suppressor cells promotes breast cancer invasion and metastasis by regulating SIRT1." Cancer Research 85, no. 8_Supplement_1 (2025): 6589. https://doi.org/10.1158/1538-7445.am2025-6589.

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Abstract Early myeloid-derived suppressor cells (eMDSCs) are a heterogeneous group of myeloid cells and have a critical role in the progression of breast cancer. Therefore, exploring the mechanism of communication between eMDSCs and tumor cells is particularly important. In this study, the results showed that eMDSCs co-incubation improved the migration and invasion ability of breast cancer cells by up-regulating the expression of microRNA(miR)-155-5p. Further, we found that eMDSCS-derived exosomes transfer miR-155-5p to breast cancer cells and down-regulate sirtuin 1(SIRT1) expression to promo

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Velázquez, Kandy T., Reilly T. Enos, Jamie L. McClellan, et al. "MicroRNA-155 deletion promotes tumorigenesis in the azoxymethane-dextran sulfate sodium model of colon cancer." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 6 (2016): G347—G358. http://dx.doi.org/10.1152/ajpgi.00326.2015.

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Clinical studies have linked microRNA-155 (miR-155) expression in the tumor microenvironment to poor prognosis. However, whether miR-155 upregulation is predictive of a pro- or antitumorigenic response is unclear, as the limited preclinical data available remain controversial. We examined miR-155 expression in tumor tissue from colon cancer patients. Furthermore, we investigated the role of this microRNA in proliferation and apoptosis, inflammatory processes, immune cell populations, and transforming growth factor-β/SMAD signaling in a chemically induced (azoxymethane-dextran sulfate sodium) m

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Kalkusova, Katerina, Pavla Taborska, Dmitry Stakheev, and Daniel Smrz. "The Role of miR-155 in Antitumor Immunity." Cancers 14, no. 21 (2022): 5414. http://dx.doi.org/10.3390/cancers14215414.

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MicroRNAs belong to a group of short non-coding RNA molecules that are involved in the regulation of gene expression at multiple levels. Their function was described two decades ago, and, since then, microRNAs have become a rapidly developing field of research. Their participation in the regulation of cellular processes, such as proliferation, apoptosis, cell growth, and migration, made microRNAs attractive for cancer research. Moreover, as a single microRNA can simultaneously target multiple molecules, microRNAs offer a unique advantage in regulating multiple cellular processes in different c

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Majewska, Aleksandra, Klaudia Brodaczewska, Aleksandra Filipiak-Duliban, Arkadiusz Kajdasz, and Claudine Kieda. "miRNA Pattern in Hypoxic Microenvironment of Kidney Cancer—Role of PTEN." Biomolecules 12, no. 5 (2022): 686. http://dx.doi.org/10.3390/biom12050686.

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MicroRNAs are post-transcriptional regulators of gene expression, and disturbances of their expression are the basis of many pathological states, including cancers. The miRNA pattern in the context of tumor microenvironment explains mechanisms related to cancer progression and provides a potential target of modern therapies. Here we show the miRNA pattern in renal cancer focusing on hypoxia as a characteristic feature of the tumor microenvironment and dysregulation of PTEN, being a major tumor suppressor. Methods comprised the CRSPR/Cas9 mediated PTEN knockout in the Renca kidney cancer cell l

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Tang, William W., H. Atakan Ekiz, Warren P. Voth, et al. "T cell expressed microRNA-155 promotes antitumor immunity and immune checkpoint blockade responses in colon cancer through repression of Ship1." Journal of Immunology 210, no. 1_Supplement (2023): 172.13. http://dx.doi.org/10.4049/jimmunol.210.supp.172.13.

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Abstract Colorectal cancer (CRC) is the 2 nddeadliest cancer globally and has the 3 rdhighest incidence and mortality in the United States. Advanced-stage disease is incurable by current clinical standards. Thus, alternative treatments are being explored, including immune checkpoint blockade (ICB) to prevent T cell inactivation by tumors. ICB induces a robust response in patients with microsatellite instability-high (MSI-H) metastatic CRC. However, most CRC patients are not responsive to ICB. Our analysis revealed MSI-H patients exhibit an immune cell-mediated inflammatory tumor microenvironme

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Zhang, Yong, Christopher P. Rombaoa, Aldo M. Roccaro, et al. "LNA Anti-MicroRNA-155: A Novel Therapeutic Strategy in Waldenstrom Macroglobulinemia and Chronic Lymphocytic Leukemia." Blood 118, no. 21 (2011): 2728. http://dx.doi.org/10.1182/blood.v118.21.2728.2728.

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Abstract Abstract 2728 Background. We and others have previously demonstrated that primary Waldenstrom's Macroglobulinemia (WM) and Chronic lymphocytic leukemia (CLL) cells show increased expression of microRNA-155 (miR-155), suggesting a role in regulating pathogenesis and tumor progression of these diseases. However, developing therapeutic agents that specifically target miRNAs has been hampered by the lack of appropriate delivery of small RNA inhibitors into tumor cells. We tested the effect of a novel LNA (locked nucleic acid)-modified anti-miR-155 in WM and CLL. Methods. WM and CLL cells,

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Koumpis, Epameinondas, Vasileios Georgoulis, Konstantina Papathanasiou, et al. "The Role of microRNA-155 as a Biomarker in Diffuse Large B-Cell Lymphoma." Biomedicines 12, no. 12 (2024): 2658. http://dx.doi.org/10.3390/biomedicines12122658.

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Diffuse Large B-cell Lymphoma (DLBCL) is the most common aggressive non-Hodgkin lymphoma (NHL). Despite the use of newer agents, such as polatuzumab vedotin, more than one-third of patients have ultimately relapsed or experienced refractory disease. MiRNAs are single-stranded, ~22-nucleotide-long RNAs that interact with their target RNA. They are significant regulators of post-transcriptional gene expression. One significant miRNA, miR-155, is involved in the pathophysiology of DLBCL and it is a critical modulator of hematopoiesis, inflammation, and immune responses. Targets of miR-155, such a

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Ramoni, Davide, and Fabrizio Montecucco. "MicroRNA-206 as a promising epigenetic approach to modulate tumor-associated macrophages in hepatocellular carcinoma." World Journal of Gastroenterology 30, no. 41 (2024): 4503–8. http://dx.doi.org/10.3748/wjg.v30.i41.4503.

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This letter comments on the recently published manuscript by Huang et al in the World Journal of Gastroenterology , which focused on the immunomodulatory effect of Calculus bovis on hepatocellular carcinoma (HCC) tumor microenvironments (TME) by inhibiting M2-tumor-associated macrophage (M2-TAM) polarization via Wnt/β-catenin pathway modulation. Recent research highlights the crucial role of TAMs and their polarization towards the M2 phenotype in promoting HCC progression. Epigenetic regulation, particularly through microRNAs (miR), has emerged as a key factor in modulating immune responses an

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Abdulla, Osama Azeldeen, Prakash S. Nagarkatti, and Mitzi Nagarkatti. "Regulation of macrophages in tumor microenvironment by microRNA in T cell lymphoma-bearing mice." Journal of Immunology 204, no. 1_Supplement (2020): 164.18. http://dx.doi.org/10.4049/jimmunol.204.supp.164.18.

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Abstract The tumor microenvironment is a complex niche created by cancer cells to survive and evade the immune system. Macrophages (Mϕs) are considered to be one of the most abundant cells in the cancer microenvironment. Studies have shown that cancer cells have predilection for the M2 cell phenotype compared to M1 in the microenvironment, because M2 Mϕs promote immunosuppression and subsequently enhance tumor cell proliferation and angiogenesis. The aim of this study was to compare the gene expression profile of tumor-associated Mϕs (TAMs) and splenic Mϕs from tumor-bearing hosts (TBHs) and d

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Renrick, Ariana N., Menaka C. Thounaojam, Portia L. Thomas, and Anil Shanker. "Bortezomib impacts Notch—miR-155 mediated augmentation of CD8+T Cell antitumor immunity." Journal of Immunology 200, no. 1_Supplement (2018): 57.2. http://dx.doi.org/10.4049/jimmunol.200.supp.57.2.

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Abstract The immunosuppressive tumor microenvironment dampens host antitumor immunity by multiple mechanisms including interference with the Notch system, which is important for various cell fate decisions and hematopoietic cell differentiation and function. We observed that treatment with bortezomib, a proteasome inhibitor, in mice bearing subcutaneous tumors resulted in an upregulated expression of various Notch signaling components in lymphoid tissues and increased CD8+T lymphocyte IFNγ secretion and expression of effector molecules, perforin and granzyme-B, as well as the T-box transcripti

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Renrick, Ariana N., Menaka Thounaojam, Evan Chaudhuri, Chandravanu Dash, and Anil Shanker. "Bortezomib improves antitumor CD8+ T cell function by modulating miR-155 and its targets." Journal of Immunology 202, no. 1_Supplement (2019): 136.18. http://dx.doi.org/10.4049/jimmunol.202.supp.136.18.

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Abstract The immunosuppressive tumor microenvironment dampens host antitumor immunity by multiple mechanisms including interfering with various cell signaling pathways that aid in the differentiation and function of immune cells. We have taken an immunotherapeutic approach in order to strengthen antitumor immunity in mice bearing solid tumors, specifically breast tumors. In doing so, we observed that treatment with bortezomib, an FDA-approved proteasome inhibitor, has the ability to increase CD8+T lymphocyte IFNγ secretion and expression of effector molecules, perforin, granzyme-B and the T-bo

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Park, Moon Nyeo, Myoungchan Kim, Soojin Lee, et al. "Targeting Redox Signaling Through Exosomal MicroRNA: Insights into Tumor Microenvironment and Precision Oncology." Antioxidants 14, no. 5 (2025): 501. https://doi.org/10.3390/antiox14050501.

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Reactive oxygen species (ROS) play a dual role in cancer progression, acting as both signaling molecules and drivers of oxidative damage. Emerging evidence highlights the intricate interplay between ROS, microRNAs (miRNAs), and exosomes within the tumor microenvironment (TME), forming a regulatory axis that modulates immune responses, angiogenesis, and therapeutic resistance. In particular, oxidative stress not only stimulates exosome biogenesis but also influences the selective packaging of redox-sensitive miRNAs (miR-21, miR-155, and miR-210) via RNA-binding proteins such as hnRNPA2B1 and SY

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Carlesso, Nadia. "Reacting to Inflammatory Signals." Blood 126, no. 23 (2015): SCI—30—SCI—30. http://dx.doi.org/10.1182/blood.v126.23.sci-30.sci-30.

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Specialized cellular niches in the bone marrow (BM) modulate critical functions of the hematopoietic stem and progenitor cells, such as self-renewal, cell-fate decisions and the balance between proliferation and differentiation. Constituents of the BM niche, such as osteoblasts, endothelial cells and macrophages, respond to inflammation with secretion of pro-inflammatory cytokines, and serve as effectors of the inflammatory circuitry; thus their excessive activation can potentially impact on the regulation of hematopoietic cells, and on the initiation and progression of myeloid malignancies. O

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Sharma, Sonali, Gabriela Mladonicka Pavlasova, Vaclav Seda, et al. "miR-29 modulates CD40 signaling in chronic lymphocytic leukemia by targeting TRAF4: an axis affected by BCR inhibitors." Blood 137, no. 18 (2021): 2481–94. http://dx.doi.org/10.1182/blood.2020005627.

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Abstract B-cell receptor (BCR) signaling and T-cell interactions play a pivotal role in chronic lymphocytic leukemia (CLL) pathogenesis and disease aggressiveness. CLL cells can use microRNAs (miRNAs) and their targets to modulate microenvironmental interactions in the lymph node niches. To identify miRNA expression changes in the CLL microenvironment, we performed complex profiling of short noncoding RNAs in this context by comparing CXCR4/CD5 intraclonal cell subpopulations (CXCR4dimCD5bright vs CXCR4brightCD5dim cells). This identified dozens of differentially expressed miRNAs, including se

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Chen, Xiaomei, Fang Liu, Wei Xiong, et al. "Comparison of miRNA Expression Profiles in Leukemia-Derived Microvesicles and Corresponding Leukemia Cells and Analysis of Their Roles in Leukemia." Blood 118, no. 21 (2011): 1388. http://dx.doi.org/10.1182/blood.v118.21.1388.1388.

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Abstract Abstract 1388 Microvesicles(MVs) are small exosomes of endocytic origin released by normal healthy or damaged cell types, including leukemic cells. MVs have been considered as cell dust, however, recent data bring evidences that MVs generated during cell activation or apoptosis can transfer biologic messages between different cell types. MicroRNAs (miRNAs) have been demonstrated to be aberrantly expressed in leukemia and the overall miRNA expression could differentiate normal versus leukemia. The MVs expressing miRNAs were found in the primary tumors. However it is currently unknown w

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Seiffert, Martina, Franziska Haderk, Laura Llao Cid, Maria Göbel, Jan Dürig та Peter Lichter. "Chronic Lymphocytic Leukemia-Derived Extracellular Vesicles Mediate NFκB Signaling and Pro-Inflammatory Cytokine Release in Monocytes". Journal of Immunology 196, № 1_Supplement (2016): 73.6. http://dx.doi.org/10.4049/jimmunol.196.supp.73.6.

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Abstract Chronic lymphocytic leukemia (CLL)is a B-cell malignancy associated with an inflammatory milieu and impairedanti-tumor immunity. This study aimed at characterizing CLL-derived extracellularvesicles (EVs) and their role in the tumor microenvironment. EVs were isolated from blood plasma or culture supernatant of the CLL cell line MEC-1 by a serialcentrifugation protocol. Characterization of EVs by electron microscopy, Nanoparticle Tracking Analysis (NTA) and Western blotting revealed vesicles 30to 350 nm in size, which were positive for various EV marker proteins. Quantificationof EVs b

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Nguyen, Grace, MinHye Noh, Yulin Dai, Zhongming Zhao, Ji Young Yoo, and Tae Jin Lee. "Abstract LB298: Simultaneous reprogramming of glioblastoma tumor cells and tumor-associated macrophages by tumor-suppressive microRNA." Cancer Research 84, no. 7_Supplement (2024): LB298. http://dx.doi.org/10.1158/1538-7445.am2024-lb298.

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Abstract Therapeutic outcomes in glioblastoma (GBM) patients remain dismal due to its resistance to conventional therapies. Tumor-supportive tumor microenvironment (TME) that is educated by tumor cells through immune editing is not properly primed for the treatment. Targeted reprogramming of both tumor cells and tumor-associated macrophages (TAMs) is expected to prime the tumor cells and the immunosuppressive TME. Tumor suppressive microRNAs (miRNAs) have been proposed as the most suitable therapeutic target to perform the tumor reprogramming role. We recently identified miR-138 as a putative

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Navarro, Alfons, Antonio Martinez, Olga Balagué, et al. "MicroRNA Analysis by In Situ Hibridization in Hodgkin Lymphoma." Blood 110, no. 11 (2007): 2271. http://dx.doi.org/10.1182/blood.v110.11.2271.2271.

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Abstract Hodgkin lymphoma (HL) is a neoplasm characterized by the presence of relatively few tumoral cells, Hodgkin and Reed-Sternberg cells in an important non-neoplastic environment. The mature microRNAs (miRNAs) are small RNA molecules (20–25 nt), that act inhibiting the mRNA translation to protein by binding to 3′ UTR region of mRNA. In a previous work we detect a 25 miRNA signature of HL. Some of them inhibit the expression of key genes related to B lymphomagenesis. The aim of the study was to determine if the differential expression of miRNAs in tumoral tissue versus reactive lymph nodes

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MUSHII, O., A. PAVLOVA, V. BAZAS, T. BORIKUN, and N. LUKIANOVA. "Mast Cells as a Factor in Regulation of Breast Cancer Stromal Component Associated with Breast Cancer Aggressiveness." Experimental Oncology 46, no. 4 (2025): 311–23. https://doi.org/10.15407/exp-oncology.2024.04.311.

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Background. It has been proven that changes in the morphology, representation, and organization of collagen fibers contribute to the formation of a unique microenvironment, which is associated with the metastatic potential of malignant neoplasms due to the initiation of cell migration and changes in polarization. Among the modulators of the collagen stroma, fibroblasts remain the most widely studied today. At the same time, much less attention is focused on the study of immune cells in the tumor microenvironment, in particular, mast cells (MCs). Aim. To investigate the relationship between the

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Jiang, Yi-Xin, Yan Chen, Yue Yang, Xiao-Xia Chen, and Dan-Dan Zhang. "Screening Five Qi-Tonifying Herbs on M2 Phenotype Macrophages." Evidence-Based Complementary and Alternative Medicine 2019 (January 15, 2019): 1–8. http://dx.doi.org/10.1155/2019/9549315.

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Tumor-associated macrophages (TAMs) with M2 phenotype play an essential role in tumor microenvironment (TME) during the progression and development of numerous cancers and associated with poor prognosis. Thus, regulation of TAMs polarization emerged as a new strategy for tumor immune therapy. According to Traditional Chinese Medicine (TCM) theory, herbs with Qi-tonifying character are involved in improving the defense capacity of immune system. In this study, we screened extracts and ingredients from five Qi-tonifying herbs exhibiting an inhibitory effect on M2 polarization of murine macrophag

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Lone, Waseem, Alyssa Bouska, Tyler Herek, et al. "Genome-Wide microRNA Expression Profiling in Molecular Subgroups of Peripheral T-Cell Lymphoma Identified Role of Mir-126 in T-Cell Lymphomagenesis." Blood 134, Supplement_1 (2019): 2767. http://dx.doi.org/10.1182/blood-2019-129327.

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Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of non-Hodgkin lymphomas and approximately 30% of PTCLs are designated as not-otherwise specified (PTCL-NOS). Gene expression profiling (GEP) identified molecular classifiers for PTCL entities and identified 2 novel biological subgroups within PTCL-NOS (PTCL-GATA3 and PTCL-TBX21), associated with T-cell differentiation subsets. To further investigate molecular oncogenesis, we performed microRNA expression profiling (miR-EP) in several molecular subtypes of PTCL including angioimmunoblastic T-cell lymphoma (AITL), PTCL-GATA3 and PTCL-TB

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Yoo, Wonbeak, Yeeun Lee, Kyung Chan Park, and Hyunji Choi. "Abstract 2353: CRHBP, a novel multiple cancer biomarker connected with better prognosis and anti-tumorigenicity." Cancer Research 85, no. 8_Supplement_1 (2025): 2353. https://doi.org/10.1158/1538-7445.am2025-2353.

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Abstract Corticotropin-releasing hormone-binding protein (CRHBP) is a key modulator of the hypothalamic-pituitary-adrenal (HPA) axis and plays a crucial role in stress responses, immune regulation, and neuroendocrine functions. Despite its importance in physiological processes, the role of CRHBP in tumor biology and its clinical relevance remain largely unknown. This study aims to comprehensively investigate CRHBP expression across diverse cancer types, its prognostic significance, and its potential molecular mechanisms in tumor progression. We show that CRHBP expression was consistently downr

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Mirza, Sheefa, Clement Penny, Nayan K. Jain, and Rakesh M. Rawal. "Curcumin mediated dendritic cell maturation by modulating cancer associated fibroblasts-derived exosomal miRNA-146a." Journal of Cancer Research and Therapeutics 19, Suppl 2 (2023): S649—S657. http://dx.doi.org/10.4103/jcrt.jcrt_1286_22.

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ABSTRACTS Background: Though cancer associated fibroblasts (CAFs), being a main component of tumor microenvironment (TME), are known to modulate immune response through secretion of various growth hormones, exosomes carrying miRNAs and cytokines; their effect on dendritic cells (DCs) are yet to be elucidated. Thus, aim of this study was to assess the effect of miRNAs and cytokines released by lung-CAFs and to evaluate immunomodulatory potential of curcumin on DC maturation through modulating their TME. Material and Methods: To check the effect of CAFs derived exosomes on DC maturation, we cult

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Cheleschi, Sara, Sara Tenti, Sauro Lorenzini та ін. "Synovial Fluid Regulates the Gene Expression of a Pattern of microRNA via the NF-κB Pathway: An In Vitro Study on Human Osteoarthritic Chondrocytes". International Journal of Molecular Sciences 23, № 15 (2022): 8334. http://dx.doi.org/10.3390/ijms23158334.

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Synovial fluid (SF) represents the primary source of nutrients of articular cartilage and is implicated in maintaining cartilage metabolism. We investigated the effects of SF, from patients with osteoarthritis (OA), rheumatoid arthritis (RA), and controls, on a pattern of microRNA (miRNA) in human OA chondrocytes. Cells were stimulated with 50% or 100% SF for 24 h and 48 h. Apoptosis and superoxide anion production were detected by cytometry; miRNA (34a, 146a, 155, 181a), cytokines, metalloproteinases (MMPs), type II collagen (Col2a1), antioxidant enzymes, B-cell lymphoma (BCL)2, and nuclear f

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McClanahan, Fabienne, Federica Calore, Nicola Zanesi, John G. Gribben, and Carlo M. Croce. "Aberrant PD-L1 Expression in CLL As a Result of Adaptive Immune Resistance Mediated By Tumor-Secreted Circulating miRNA Binding to Toll-like Receptor 7." Blood 124, no. 21 (2014): 716. http://dx.doi.org/10.1182/blood.v124.21.716.716.

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Abstract Background: Chronic lymphocytic leukaemia (CLL) is a model cancer to study immune evasion via PD-L1/PD-1 signalling: aberrantly expressed PD-L1 on CLL and PD-1 on CD8 T cells are key mediators of poor anti-tumor immune responses, which are a major hallmark of CLL. Several preclinical studies suggest that aberrant PD-L1 expression is a result of adaptive immune resistance and is induced during immune responses within the tumor microenvironment. It has recently been proposed that specific circulating microRNAs (miRNAs) shed by malignant cells participate in the complex crosstalk between

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Tsukamoto, Shokichi, Karma Salem, Salomon Manier, et al. "Microrna-138 Regulates Osteogenic Differentiation and Its Inhibition Presents a Novel Therapeutic Line to Prevent Bone Lytic Lesions in Multiple Myeloma." Blood 128, no. 22 (2016): 4483. http://dx.doi.org/10.1182/blood.v128.22.4483.4483.

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Abstract Introduction The bone marrow (BM) microenvironment in multiple myeloma (MM) plays a pivotal role in tumor growth and bone destructive process. Mesenchymal stromal cells (MSCs) in MM exhibit different genomic and cytokine secretion profiles that ultimately impair their osteogenic differentiation abilities compared to normal MSCs. However, the underlying molecular mechanisms are not fully understood. In the present study, we explored the role of miR-138 in MSCs derived from MM patients (MM-MSCs) and the potential for anti-miR-138 treatment to rescue impaired osteogenic differentiation i

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Dubois, Nathan, David Van Morkhoven, Laurentijn Tilleman, et al. "Extracellular Vesicles from Chronic Lymphocytic Leukemia Cells Promote Leukemia Aggressiveness By Inducing the Differentiation of Monocytes into Nurse-like Cells Via an RNA-Dependent Mechanism." Blood 144, Supplement 1 (2024): 3229. https://doi.org/10.1182/blood-2024-194217.

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Background: Bidirectional interactions exist between Chronic Lymphocytic Leukemia (CLL) cells and the cells of their microenvironment (ME): CLL cells indeed received several stimuli such as BCR stimulation but they can also interact with the surrounding cells by the release of extracellular vesicles (EVs). EVs are small double membrane particles (from 100nm to 1µm) carrying proteins, DNA and several types of RNA such as microRNAs or Y RNAs. EV exchange is today considered as a new way of cellular communication. Methods: The small RNA profile (microRNA and Y RNA) of CLL-EVs isolated by ultracen

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Youness, R. A., та A. Abdelmotaal. "13P A mitigation of breast cancer-induced immune-suppressive tumor microenvironment through curbing miR-155/IL-10/TNF-α loop using a novel quercetin derivative". Annals of Oncology 31 (березень 2020): S4. http://dx.doi.org/10.1016/j.annonc.2020.01.061.

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Piltan, Samira, Humna Hasan, Ikjot Sohal, et al. "Abstract 1192: Selective sorting of tumor suppressive and oncogenic miRNAs into extracellular vesicles: Implications for cancer progression." Cancer Research 85, no. 8_Supplement_1 (2025): 1192. https://doi.org/10.1158/1538-7445.am2025-1192.

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Abstract Lung cancer remains the leading cause of cancer-related deaths worldwide, largely due to late diagnoses often coinciding with advanced, metastatic stages. Thus, a deeper understanding of the tumor microenvironment (TME) and the molecular mechanisms driving cancer progression and metastasis is critical. Among the many contributors to the TME, extracellular vesicles (EVs) are crucial in facilitating intercellular communication, enabling the transport of biomolecules such as lipids, RNAs, DNA, and proteins. Of the various biomolecules, microRNAs (miRNAs) have emerged as crucial regulator

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Abdelhamed, Sherif, Noah I. Hornick, and Peter Kurre. "Residual HSPC in the Leukemia Microenvironment Are Reprogrammed Via Extracellular Vesicle Trafficking." Blood 128, no. 22 (2016): 888. http://dx.doi.org/10.1182/blood.v128.22.888.888.

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Several groups have shown that leukemic cells create a self-reinforcing bone marrow (BM) niche that functionally impairs normal hematopoietic stem and progenitor cells (HSPC) indirectly through stroma-secreted factors. We recently demonstrated an alternative mechanism whereby extracellular vesicles (EVs) from acute myeloid leukemia (AML) patients and cell lines, but not BM CD34 controls, suppress their clonogenicity through EV trafficking of microRNA that directly downregulate critical transcription factors (c-Myb and HoxA9). Here, we aimed to clarify the fate of residual HSPC in in vivo AML x

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Hasan, Humna, Nadia A. Lanman, Sagar Utturkar, and Andrea L. Kasinski. "Abstract 1537: Understanding role of uniquely enriched RNAs carried in non-small cell lung cancer derived extracellular vesicles and dynamics of their selective export." Cancer Research 82, no. 12_Supplement (2022): 1537. http://dx.doi.org/10.1158/1538-7445.am2022-1537.

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Abstract The dynamic interaction mediated by extracellular vesicles (EVs) between cancer cells and microenvironment has been shown to regulate cancer progression. Specifically, tumor derived EVs alter the phenotypes of recipient cells by delivering functional biomolecules including RNAs (EV-RNA). Studies from our lab reveal the impact of NSCLC derived EVs (Calu6 and H358) in promoting invasion of non-tumorigenic cells (BEAS-2B) and disruption of an epithelial barrier. We further determined that of all the major macromolecules contained in EVs, EV-RNA is a significant contributor to the observe

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Haderk, Franziska, Etienne Moussay, Jerome Paggetti, et al. "Chronic Lymphocytic Leukemia-Derived Extracellular Vesicles Contain a Distinctive Proteome, As Well As Specific Micro RNAs and Y RNAs." Blood 124, no. 21 (2014): 1968. http://dx.doi.org/10.1182/blood.v124.21.1968.1968.

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Abstract The pathogenesis of chronic lymphocytic leukemia (CLL) is stringently associated with a tumor-supportive microenvironment and a dysfunctional immune system. Of note, CLL cells themselves induce changes in surrounding cells, and extracellular vesicles (EVs) released by CLL cells represent a newly discovered mechanism of cell-cell communication. EVs are membrane enclosed nanoparticles 30 to 1000 nm in size and are able to reprogram recipient cells by transferring proteins and RNA molecules from their cell of origin. Thus, we aimed to analyze CLL cell-derived EVs present in blood plasma

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Wang, Xinyi, Jiemeng Zhang, Yingluo Liu, et al. "Abstract 2274: Genomic and transcriptomic analyses of chemical hepatocarcinogenesis aggravated by loss of oncoproteins in hepatocytes." Cancer Research 84, no. 6_Supplement (2024): 2274. http://dx.doi.org/10.1158/1538-7445.am2024-2274.

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Abstract Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death without effective treatment. Oncogenic drivers, including PTPN11/Shp2, Ikkβ kinase (IKK), c-Met and β-catenin, as well as tumor microenvironment as illustrated by a carcinogen or diethylnitrosamine (DEN)-treated models, have combined contribution to cancer progression that have distinct prevalence in human HCC progression. We previously found that disruption of Ras/Erk by Shp2 deletion combined with deletion of NF-κB unexpectedly dysregulated circadian clock genes which leads to further cancer prog

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Villalobos-Ayala, Krystal, Valentina Laverde, Jennifer Permuth, et al. "Abstract C043: SHIP-1: Therapeutic target to reduce health disparities in African Americans with pancreatic cancer." Cancer Epidemiology, Biomarkers & Prevention 32, no. 12_Supplement (2023): C043. http://dx.doi.org/10.1158/1538-7755.disp23-c043.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers and African Americans (AA) have higher mortality rates compared to European Americans (EA) due to heighten inflammation which is known to be regulated by Src-homology inositol phosphatase-1 (SHIP-1). SHIP-1 is a master regulator of macrophage development and function which impacts tumor immunity and thus can be a therapeutic target that may explain treatment failure, which contributes to health disparity associated with AA vs. EA with PDAC. We reported that SHIP-1 expression is vital for the expansion of tumoricid

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