Journal articles: 'MiR-202'

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Lin, Yilin, Zhihua Chen, Suyong Lin, Yan Zheng, Yisu Liu, Ji Gao, and Shaoqin Chen. "MiR-202 inhibits the proliferation and invasion of colorectal cancer by targeting UHRF1." Acta Biochimica et Biophysica Sinica 51, no. 6 (May 6, 2019): 598–606. http://dx.doi.org/10.1093/abbs/gmz042.

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Abstract The purpose of this study was to investigate the expression of microRNA-202 (miR-202) and its role in colorectal cancer (CRC) in vivo and in vitro. We examined the expression of miR-202 in CRC tissues by quantitative real-time PCR (qRT-PCR) assay. Lentiviral vectors were constructed to overexpress or inhibit the expression of miR-202 in the CRC cell lines HCT116 and SW480 to determine its effects on cell invasion and proliferation. We found that overexpression of miR-202 significantly inhibited the proliferation and invasion of HCT116 cells. MiRNA target gene prediction, dual luciferase assay, and western blot analysis demonstrated that miR-202 regulated ubiquitin-like with PHD and RING finger domain 1 (UHRF1) expression in both cell lines. The effect of miR-202 on cell proliferation and invasion was partially reversed by activating the expression of UHRF1. Furthermore, miR-202 induced tumor formation in HCT116 xenograft BALB/c nude mice. Mice vaccinated with miR-202-overexpressing cells had smaller tumors and lower UHRF1 expression than the control group. These results indicate the possibility that miR-202 is under-expressed in CRC tissues, and that miR-202 inhibits the proliferation and invasion of CRC via targeting UHRF1. MiR-202 is a potential therapeutic target for CRC.

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Zhang, Liqing, Jianjiang Xu, Gaodi Yang, Heng Li, and Xiuxia Guo. "miR-202 Inhibits Cell Proliferation, Migration, and Invasion by Targeting Epidermal Growth Factor Receptor in Human Bladder Cancer." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 26, no. 6 (July 5, 2018): 949–57. http://dx.doi.org/10.3727/096504018x15149787144385.

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Recent studies have demonstrated that miR-202 is associated with several types of cancer; however, the expression and function of miR-202 have not been investigated in bladder cancer. We analyzed the expression of miR-202 in bladder cancer tissues and adjacent noncancerous tissues. The effect of miR-202 on the proliferation, migration, and invasion was evaluated by in vitro assays. The target gene of miR-202 was assessed by luciferase reporter assay. In this study, miR-202 was found to be significantly downregulated in bladder cancer cell lines and tissues and was highly correlated with the T classification, N classification, grade, and recurrence. Ectopic expression of miR-202 suppressed cell viability, colony formation, cell migration, and invasion in vitro and inhibited xenograft tumor growth in vivo. Inversely, downregulation of miR-202 had contradictory effects. The 3′-untranslated region (3′-UTR) of epidermal growth factor receptor (EGFR) was identified as a direct target of miR-202 using luciferase reporter assays, and knockdown of EGFR enhanced miR-202-inhibited cell proliferation, migration, and invasion. In conclusion, miR-202 suppresses bladder cancer carcinogenesis and progression by targeting EGFR, thereby representing a potential target for miRNA-based therapy for bladder cancer in the future.

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Deng, Xinchao, Congzhe Hou, Zhen Liang, Huali Wang, Lin Zhu, and Hui Xu. "miR-202 Suppresses Cell Proliferation by Targeting FOXR2 in Endometrial Adenocarcinoma." Disease Markers 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/2827435.

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Background. MicroRNA-202 (miR-202) has been reported to be aberrantly regulated in several cancers. The aim of this study is to explore the functional role of miR-202 in EAC tumor growth. Material and Methods. miR-202 expression was detected by qRT-PCR. TargetScan and luciferase reporter assay were used to elucidate the candidate target gene of miR-202. The FOXR2 protein level was assessed by Western blot and immunohistochemistry. Survival analysis was explored for FOXR2 expression in EAC patients. Results. miR-202 expression was significantly decreased in EAC tissues (P<0.01) compared with that in control tissues. And the downregulate miR-202 was significantly associated with poor prognosis (P<0.01). Re-expression of miR-202 dramatically suppressed cell proliferation in vitro and tumor growth in vivo. FOXR2 was identified as a direct target of miR-202. In EAC tissues, FOXR2 was upregulated and the increased FOXR2 was significantly associated with poor prognosis. In miR-202-transfected cells, the FOXR2 expression was inversely changed. The analysis of FOXR2 protein expression and miR-202 transcription in EAC tissues showed negative correlation (R=−0.429). Conclusion. miR-202 may function as a tumor suppressor in EAC tumor growth by targeting FOXR2 oncogene, which may provide new insights into the molecular mechanism and new targets for treatment of EAC.

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Zhuang, Donghai, Li Liang, Hongzhan Zhang, and Xianguang Feng. "miR-202 Suppresses Hepatocellular Carcinoma Progression via Downregulating BCL2 Expression." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 28, no. 4 (September 1, 2020): 399–408. http://dx.doi.org/10.3727/096504020x15864296270581.

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miRNAs play an important role in progression of hepatocellular carcinoma (HCC). In this work, we assessed the function of miR-202 in human HCC and identified BCL2 as its target. We found miR-202 expression was found significantly downregulated, while BCL2 expression was markedly upregulated in HCC tissues and cell lines (HepG2, Hep3B, and HCCLM3). Both miR-202 and BCL2 were closely correlated with major vascular invasion and advanced TNM stage as well as overall survival of HCC patients. Overexpression of miR-202 significantly inhibited cell proliferation, induced apoptosis and cell cycle arrest at the G0/G1 phase, and prevented tumor formation in a xenograft nude mouse model. Further, miR-202 dramatically inhibited migration, invasion, and epithelialmesenchymal transition. miR-202 bound to the 3-untranslated region (3-UTR) of BCL2 mRNA and downregulated the expression level of BCL2 protein. Exogenous BCL2 overexpression weakened the inhibitory effects of miR-202, while inhibition of BCL2 enhanced the inhibitory effects of miR-202. In conclusion, miR-202 serves as a tumor suppressor in HCC progression by downregulating BCL2 expression, indicating miR-202 might be a potential target for HCC.

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WANG, Qifeng, and Xiang Du. "Effect of microRNA-202-3p on cell proliferation and targeting of ADP-ribosylation factor-like 5A in human colorectal carcinoma." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e14667-e14667. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e14667.

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e14667 Background: MicroRNAs (miRNAs) are small, non-coding RNAs that are strongly implicated in cancer and reshaped our understanding of the role of non-protein-coding genes in carcinogenesis. Methods: Quantitative RT-PCR was used to evaluate miR-202-3p expression in 94 pairs of human primary CRC and adjacent noncancerous tissues (NCT) to determine the clinicopathologic significance of miR-202-3p. Cell proliferation analysis and Xenograft analysis was used to investigate miR-202-3p function in vitro and in vivo.It’s direct target ARL5A was confirmed by Luciferase assay and Western blot. Immunochemistry was performed to reveal endogenous protein level of ARL5A and analysis clinical significance. Results: In this study, miR-202-3p was verified significantly down regulated in 46.7% (44/94) of the CRC tissues when compared to the corresponding noncancerous tissues(NCT). Subsequently, DNA copy number deletion of Pre-miR-202 in 63.2%(24/38) CRC tissue was proved(compared with NCT), which was considered as a main cause of the low expression of miR-202-3p. Cell proliferation analysis and colony formation assay showed that overexpression of miR-202-3p inhibit CRC cell growth in vitro. Xenograft analysis revealed that ectopic expression of miR-202-3p decreased the tumorigenicity of CRC cells in vivo. Consistent with these results, silencing of miR-202-3p resulted in a increased growth ratio of the colon cancer cells. In addition, ADP-ribosylation factor-like 5A(ARL5A) was predicted as potential target of miR-202-3p which was confirmed by Luciferase assay and Western blot. Overexpression of miR-202-3p could reduced the endogenous protein level of ARL5A, whereas silencing of miR-202-3p obviously up regulated ARL5A expression. In human CRC tissues, miR-202-3p expression levels correlated inversely with ARL5A protein levels which was identified as an prognostic factor in this study. Furthermore, knockdown of ARL5A phenocopied the proliferation-inhibiting effect of miR-202-3p. Conclusions: These results indicated that miR-202-3p, acting as a new tumor suppressor in CRC, could decrease cell proliferation via directly targeting ARL5A, a first reported gene related to CRC prognosis.

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Ding, Qiang, Miaohan Jin, Yaoyue Wang, Jiao Liu, Peter Kalds, Ying Wang, Yuxin Yang, Xiaolong Wang, and Yulin Chen. "Transactivation of miR-202-5p by Steroidogenic Factor 1 (SF1) Induces Apoptosis in Goat Granulosa Cells by Targeting TGFβR2." Cells 9, no. 2 (February 14, 2020): 445. http://dx.doi.org/10.3390/cells9020445.

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MicroRNAs play key roles during ovary development, with emerging evidence suggesting that miR-202-5p is specifically expressed in female animal gonads. Granulosa cells (GCs) are somatic cells that are closely related to the development of female gametes in mammalian ovaries. However, the biological roles of miR-202-5p in GCs remain unknown. Here, we show that miR-202-5p is specifically expressed in GCs and accumulates in extracellular vesicles (EVs) from large growth follicles in goat ovaries. In vitro assays showed that miR-202-5p induced apoptosis and suppressed the proliferation of goat GCs. We further revealed that miR-202-5p is a functional miRNA that targets the transforming growth factor-beta type II receptor (TGFβR2). MiR-202-5p attenuated TGF-β/SMAD signaling through the degradation of TGFβR2 at both the mRNA and protein level, decreasing p-SMAD3 levels in GCs. Moreover, we verified that steroidogenic factor 1 (SF1) is a transcriptional factor that binds to the promoters of miR-202 and cytochrome P450 family 19 subfamily A member 1 (CYP19A1) through luciferase reporter and chromatin immunoprecipitation (ChIP) assays. That contributed to positive correlation between miR-202-5p and CYP19A1 expression and estradiol (E2) release. Furthermore, SF1 repressed TGFβR2 and p-SMAD3 levels in GCs through the transactivation of miR-202-5p. Taken together, these results suggest a mechanism by which miR-202-5p regulates canonical TGF-β/SMAD signaling through targeting TGFβR2 in GCs. This provides insight into the transcriptional regulation of miR-202 and CYP19A1 during goat ovarian follicular development.

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Ahmed, Emad A., Peramaiyan Rajendran, and Harry Scherthan. "The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor." International Journal of Molecular Sciences 23, no. 11 (May 24, 2022): 5870. http://dx.doi.org/10.3390/ijms23115870.

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MicroRNA-202 (miR-202) is a member of the highly conserved let-7 family that was discovered in Caenorhabditis elegans and recently reported to be involved in cell differentiation and tumor biology. In humans, miR-202 was initially identified in the testis where it was suggested to play a role in spermatogenesis. Subsequent research showed that miR-202 is one of the micro-RNAs that are dysregulated in different types of cancer. During the last decade, a large number of investigations has fortified a role for miR-202 in cancer. However, its functions can be double-edged, depending on context they may be tumor suppressive or oncogenic. In this review, we highlight miR-202 as a potential diagnostic biomarker and as a suppressor of tumorigenesis and metastasis in several types of tumors. We link miR-202 expression levels in tumor types to its involved upstream and downstream signaling molecules and highlight its potential roles in carcinogenesis. Three well-known upstream long non-coding-RNAs (lncRNAs); MALAT1, NORAD, and NEAT1 target miR-202 and inhibit its tumor suppressive function thus fueling cancer progression. Studies on the downstream targets of miR-202 revealed PTEN, AKT, and various oncogenes such as metadherin (MTDH), MYCN, Forkhead box protein R2 (FOXR2) and Kirsten rat sarcoma virus (KRAS). Interestingly, an upregulated level of miR-202 was shown by most of the studies that estimated its expression level in blood or serum of cancer patients, especially in breast cancer. Reduced expression levels of miR-202 in tumor tissues were found to be associated with progression of different types of cancer. It seems likely that miR-202 is embedded in a complex regulatory network related to the nature and the sensitivity of the tumor type and therapeutic (pre)treatments. Its variable roles in tumorigenesis are mediated in part thought its oncogene effectors. However, the currently available data suggest that the involved signaling pathways determine the anti- or pro-tumorigenic outcomes of miR-202’s dysregulation and its value as a diagnostic biomarker.

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Kim, Jungho, Sunyoung Park, Dasom Hwang, Seung Il Kim, and Hyeyoung Lee. "Diagnostic Value of Circulating miR-202 in Early-Stage Breast Cancer in South Korea." Medicina 56, no. 7 (July 9, 2020): 340. http://dx.doi.org/10.3390/medicina56070340.

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Background and objectives: Breast cancer is the most common cancer among women worldwide. Early stage diagnosis is important for predicting increases in treatment success rates and decreases in patient mortality. Recently, circulating biomarkers such as circulating tumor cells, circulating tumor DNA, exosomes, and circulating microRNAs have been examined as blood-based markers for the diagnosis of breast cancer. Although miR-202 has been studied for its function or expression in breast cancer, its potential diagnostic value in a clinical setting remains elusive and miR-202 has not been investigated in South Korea. In this study, we aimed to evaluate the diagnostic utility of miR-202 in plasma samples of breast cancer patients in South Korea. Materials and Methods: We investigated miR-202 expression in the plasma of 30 breast cancer patients during diagnosis along with 30 healthy controls in South Korea by quantitative reverse transcription PCR. Results: The results showed that circulating miR-202 levels were significantly elevated in the breast cancer patients compared with those in healthy controls (p < 0.001). The sensitivity and specificity of circulating miR-202 were 90.0% and 93.0%, respectively. Additionally, circulating miR-202 showed high positivity at early stage. The positive rate of miR-202 was as follows: 100% (10/10) for stage I, 90% (9/10) for stage II, and 80% (8/10) for stage III. miR-202 was also a predictor of a 9.6-fold high risk for breast cancer (p < 0.001). Conclusions: Additional alternative molecular biomarkers for diagnosis and management of pre-cancer patients are needed. Circulating miR-202 might be potential diagnostic tool for detecting early stage breast cancer.

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Mo, Chengyu, Wenjing Li, Kuntong Jia, Wei Liu, and Meisheng Yi. "Proper Balance of Small GTPase rab10 Is Critical for PGC Migration in Zebrafish." International Journal of Molecular Sciences 22, no. 21 (November 4, 2021): 11962. http://dx.doi.org/10.3390/ijms222111962.

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MicroRNAs (miRNAs) play important roles in post-transcriptional repression in nearly every biological process including germ cell development. Previously, we have identified a zebrafish germ plasm-specific miRNA miR-202-5p, which regulates PGC migration through targeting cdc42se1 to protect cdc42 expression. However, knockdown of cdc42se1 could not significantly rescue PGC migration in maternal miR-202 mutant (MmiR-202) embryos, indicating that there are other target genes of miR-202-5p required for the regulation of PGC migration. Herein, we revealed the transcriptional profiles of wild type and MmiR-202 PGCs and obtained 129 differentially expressed genes (DEGs), of which 42 DEGs were enriched cell migration-related signaling pathways. From these DEGs, we identified two novel miR-202-5p target genes prdm12b and rab10. Furthermore, we found that disruption of rab10 expression led to significantly migratory defects of PGC by overexpression of rab10 siRNA, or WT, inactive as well as active forms of rab10 mRNA, and WT rab10 overexpression mediated migratory defects could be partially but significantly rescued by overexpression of miR-202-5p, demonstrating that rab10 is an important factor involved miR-202-5p mediated regulation of PGC migration. Taken together, the present results provide significant information for understanding the molecular mechanism by which miR-202-5p regulates PGC migration in zebrafish.

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Sun, Wei, Wei Ping, Yitao Tian, Wenbin Zou, Jiawei Liu, and Yukun Zu. "miR-202 Enhances the Anti-Tumor Effect of Cisplatin on Non-Small Cell Lung Cancer by Targeting the Ras/MAPK Pathway." Cellular Physiology and Biochemistry 51, no. 5 (2018): 2160–71. http://dx.doi.org/10.1159/000495835.

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Background/Aims: KRas is usually mutated in non-small cell lung cancer (NSCLC). The mutated KRas gene is a negative prognostic indicator that promotes tumor proliferation, metastasis, and drug resistance in NSCLC, and thus has become a target for cancer therapy. This study is focused on the effects of the microRNA (miR)-202/KRas axis in regulating chemosensitivity in NSCLC. Methods: Quantitative reverse transcriptase real-time PCR analysis was performed to examine the expression of miR-202. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays were performed to evaluate the sensitivity of cisplatin against NSCLC cells. The miR-202/KRas axis was confirmed by western blot and luciferase reporter assays. Cell apoptosis was measured by flow cytometry. KRas expression, MEK1/2 and ERK1/2 phosphorylation, and activation of caspase-9 and caspase-3 were detected by western blot. Results: A significant decrease in miR-202 expression was observed in NSCLC cells both in vivo and in vitro. In addition, miR-202 expression was associated with drug resistance. Recovery of miR-202 expression levels was found to increase the sensitivity of both NCI-H441 and A549 NSCLC cells to cisplatin treatment. Mechanically, as the Ras/mitogen-activated protein kinase (MAPK) pathway was aberrantly activated in NCI-H441 and A549 NSCLC cells, the overexpression of miR-202 was found to inhibit the Ras/MAPK pathway by targeting the KRas gene. As a result, increased miR-202 expression expanded apoptosis signaling induced by cisplatin in NSCLC cells. Conclusion: The miR-202/KRas axis controlled the chemosensitivity of NSCLC by mediating the Ras/MAPK pathway. Thus, the combination of platinum-based drugs with miR-202 may represent a novel strategy to enhance the anti-tumor effect against NSCLC.

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Wei, Xiaoling, Lingjun Dong, and Xiubing Lei. "LncRNA NORAD/miR 202 5p regulates hepatoma cell viability, apoptosis via EGFR/PI3K/AKT signaling pathway." Tropical Journal of Pharmaceutical Research 22, no. 4 (May 11, 2023): 749–57. http://dx.doi.org/10.4314/tjpr.v22i4.6.

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Purpose: To examine the potential modulatory mechanisms of NORAD in hepatoma in vitro. Methods: In this study, four human hepatoma cell lines (Bel7404, PLC5, HepG2, and HuH7), as well as a human immortalized Normal MIHA cell line were employed. Transfection was performed to up-or down-regulate NORAD and miR-202-5p expression in cells. RT-qPCR was used to measure expressions of NORAD, miR-202-5p, and biomarkers for cell cycle and apoptosis in HCC cell lines. CCK-8, Flow Cytometry for apoptosis and cell cycle arrest and Western blot experiments were performed to determine cellular viability, cell cycle arrest and apoptosis and related protein expressions. Bioinformatics tool was used to find possible binding sites on NORAD and miR-202-5p, which were further validated by dual-luciferase reporter gene assays. Results: NORAD adversely modulated miR-202-5p in hepatoma cells and mediated cell viability, apoptosis and cell cycle arrest through regulatingmiR-202-5p. Functional experiments revealed that downregulation of NORAD or upregulation of miR-202-5p suppressed cell viability and inhibited apoptosis and cell cycle arrest. Silenced NORAD regulated the EGFR/PI3K/AKT pathway via enhancing miR-202-5p expression in HCC cell lines. Conclusion: NORAD interaction with miR-202-5p mediated the EGFR/PI3K/AKT network.

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Chen, Yueyao, Shiqun Zhou, and Haixiang Li. "Changes of Serum miR-202-3p Level and Its Correlation with Prognosis in Patients with Acute Kidney Injury Induced by Sepsis." Tobacco Regulatory Science 7, no. 4 (July 31, 2021): 674–82. http://dx.doi.org/10.18001/trs.7.4.1.20.

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To investigate the changes of serum miR-202-3p level and its correlation with prognosis in patients with acute kidney injury (AKI) induced by sepsis. From April 2017 to January 2019, 66 patients with AKI induced by sepsis in our hospital and 70 healthy people in the same period were selected as the research objects. The levels of miR-202-3p, BUN and Cr in serum were tested. Subsequently, cell experiments were carried out to verify the effects of the decrease of miR-202-3p level on BUN, Cr and cell growth and apoptosis. The risk factors were analysed. Compared with healthy volunteers, patients with AKI induced by sepsis had higher levels of miR-202-3p, BUN and Cr in serum. When miR-202-3p level was knocked down, the levels of BUN and Cr were declined, cell growth was improved and apoptosis rate was decreased. The risk factors were analysed, and the results revealed that miR-202-3p, BUN and Cr were independent risk factors for poor prognosis in patients with AKI induced by sepsis. The level of miR-202-3p is elevated in patients with AKI induced by sepsis, which may be a potential biomarker for diagnosis and prognosis of patients with AKI induced by sepsis.

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Liu, Wei, Yilin Jin, Wanwan Zhang, Yangxi Xiang, Peng Jia, Meisheng Yi, and Kuntong Jia. "MiR-202-5p Inhibits RIG-I-Dependent Innate Immune Responses to RGNNV Infection by Targeting TRIM25 to Mediate RIG-I Ubiquitination." Viruses 12, no. 3 (February 27, 2020): 261. http://dx.doi.org/10.3390/v12030261.

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The RIG-I-like receptors (RLRs) signaling pathway is essential for inducing type I interferon (IFN) responses to viral infections. Meanwhile, it is also tightly regulated to prevent uncontrolled immune responses. Numerous studies have shown that microRNAs (miRNAs) are essential for the regulation of immune processes, however, the detailed molecular mechanism of miRNA regulating the RLRs signaling pathway remains to be elucidated. Here, our results showed that miR-202-5p was induced by red spotted grouper nervous necrosis virus (RGNNV) infection in zebrafish. Overexpression of miR-202-5p led to reduced expression of IFN 1 and its downstream antiviral genes, thus facilitating viral replication in vitro. In comparison, significantly enhanced levels of IFN 1 and antiviral genes and significantly low viral burden were observed in the miR-202-5p-/- zebrafish compared to wild type zebrafish. Subsequently, zebrafish tripartite motif-containing protein 25 (zbTRIM25) was identified as a target of miR-202-5p in both zebrafish and humans. Ectopic expression of miR-202-5p suppressed zbTRIM25-mediated RLRs signaling pathway. Furthermore, we showed that miR-202-5p inhibited zbTRIM25-mediated zbRIG-I ubiquitination and activation of IFN production. In conclusion, we demonstrate that RGNNV-inducible miR-202-5p acts as a negative regulator of zbRIG-I-triggered antiviral innate response by targeting zbTRIM25. Our study reveals a novel mechanism for the evasion of the innate immune response controlled by RGNNV.

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Ran, Mingxia, Shenqiang Hu, Qingyuan Ouyang, Hengli Xie, Xi Zhang, Yueyue Lin, Xuejian Li, et al. "miR-202-5p Inhibits Lipid Metabolism and Steroidogenesis of Goose Hierarchical Granulosa Cells by Targeting ACSL3." Animals 13, no. 3 (January 17, 2023): 325. http://dx.doi.org/10.3390/ani13030325.

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miRNAs are critical for steroidogenesis in granulosa cells (GCs) during ovarian follicular development. We have previously shown that miR-202-5p displays a stage-dependent expression pattern in GCs from goose follicles of different sizes, suggesting that this miRNA could be involved in the regulation of the functions of goose GCs; therefore, in this study, the effects of miR-202-5p on lipid metabolism and steroidogenesis in goose hierarchical follicular GCs (hGCs), as well as its mechanisms of action, were evaluated. Oil Red O staining and analyses of intracellular cholesterol and triglyceride contents showed that the overexpression of miR-202-5p significantly inhibited lipid deposition in hGCs; additionally, miR-202-5p significantly inhibited progesterone secretion in hGCs. A bioinformatics analysis and luciferase reporter assay indicated that Acyl-CoA synthetase long-chain family member 3 (ACSL3), which activates long-chain fatty acids for the synthesis of cellular lipids, is a potential target of miR-202-5p. ACSL3 silencing inhibited lipid deposition and estrogen secretion in hGCs. These data suggest that miR-202-5p exerts inhibitory effects on lipid deposition and steroidogenesis in goose hGCs by targeting the ACSL3 gene.

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Feng, Guanghang, Jie Liu, Zitao Lu, Yaokun Li, Ming Deng, Guangbin Liu, Baoli Sun, Yongqing Guo, Xian Zou, and Dewu Liu. "miR-450-5p and miR-202-5p Synergistically Regulate Follicle Development in Black Goat." International Journal of Molecular Sciences 24, no. 1 (December 26, 2022): 401. http://dx.doi.org/10.3390/ijms24010401.

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Follicle maturation is a complex biological process governed by numerous factors, and researchers have observed follicle development by studying the proliferation and apoptosis of follicular granulosa cells (GCs). However, the regulatory mechanisms of GCs proliferation and death during follicle development are largely unknown. To investigate the regulatory mechanisms of lncRNAs, mRNAs, and microRNAs, RNA sequencing (RNA-seq) and small RNA-seq were performed on large (>10 mm) and small follicles (<3 mm) of Leizhou black goat during estrus. We discovered two microRNAs, miR-450-5p and miR-202-5p, which can target GCs in goats and may be involved in follicle maturation, and the effects of miR-450-5p and miR-202-5p on ovarian granulosa cell lines were investigated (KGN). Using cell counting kit-8 (CCK-8) assays, 5-Ethynyl-2’-deoxyuridine (EdU) assay and flow cytometry, miR-202-5p overexpression could suppress the proliferation and induce apoptosis of GCs, whereas miR-450-5p overexpression induced the opposite effects. The dual-luciferase reporter assay confirmed that miR-450-5p could directly target the BMF gene (a BCL2 modifying factor), and miR-202-5p targeted the BCL2 gene. A considerable rise in phosphorylated Akt (p-AKT) protein was observed following the downregulation of BMF by miR-450-5p mimics. After BMF gene RNAi therapy, a notable elevation in p-AKT was detected. Mimics of miR-202-5p inhibited BCL2 protein expression, significantly decreasing p-AMPK protein expression. These results imply that during the follicular development in black goats, the miR-450-5p-BMF axis favored GC proliferation on a wide scale, while the miR-202-5p-BCL2 axis triggered GC apoptosis.

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Ran, Mingxia, Shenqiang Hu, Hengli Xie, Qingyuan Ouyang, Xi Zhang, Yueyue Lin, Xin Yuan, et al. "MiR-202-5p Regulates Geese Follicular Selection by Targeting BTBD10 to Regulate Granulosa Cell Proliferation and Apoptosis." International Journal of Molecular Sciences 24, no. 7 (April 5, 2023): 6792. http://dx.doi.org/10.3390/ijms24076792.

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The regulation of granulosa cells (GCs) proliferation and apoptosis is the key step in follicular selection which determines the egg production performance of poultry. miR-202-5p has been reported to be involved in regulating the proliferation and apoptosis of mammalian ovarian GCs. However, its role in regulating the proliferation and apoptosis of goose GCs is still unknown. In the present study, the GCs of pre-hierarchical follicles (phGCs, 8–10 mm) and those of hierarchical follicles (hGCs, F2–F4) were used to investigate the role of miR-202-5p in cell proliferation and apoptosis during follicle selection. In phGCs and hGCs cultured in vitro, miR-202-5p was found to negatively regulate cell proliferation and positively regulate cell apoptosis. The results of RNA-seq showed that BTB Domain Containing 10 (BTBD10) is predicted to be a key target gene for miR-202-5p to regulate the proliferation and apoptosis of GCs. Furthermore, it is confirmed that miR-202-5p can inhibit BTBD10 expression by targeting its 3′UTR region, and BTBD10 was revealed to promote the proliferation and inhibit the apoptosis of phGCs and hGCs. Additionally, co-transfection with BTBD10 effectively prevented miR-202-5p mimic-induced cell apoptosis and the inhibition of cell proliferation. Meanwhile, miR-202-5p also remarkably inhibited the expression of Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Beta (PIK3CB) and AKT Serine/Threonine Kinase 1 (AKT1), while it was significantly restored by BTBD10. Overall, miR-202-5p suppresses the proliferation and promotes the apoptosis of GCs through the downregulation of PIK3CB/AKT1 signaling by targeting BTBD10 during follicular selection. Our study provides a theoretical reference for understanding the molecular mechanism of goose follicular selection, as well as a candidate gene for molecular marker-assisted breeding to improve the geese’ egg production performance.

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Zheng, Li, Dai Fei Sun, and Yanyan Tong. "Exosomal miR-202 derived from leukorrhea as a potential biomarker for endometriosis." Journal of International Medical Research 51, no. 1 (January 2023): 030006052211471. http://dx.doi.org/10.1177/03000605221147183.

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Objective Endometriosis (EMS) is a chronic gynecological disorder with an urgent need of a reliable non-invasive diagnostic strategy. Recently, there has been increasing interest in using the contents of exosomes, especially exosomal microRNAs (miRNAs), as potential biomarkers for various types of diseases. In this study, we assessed the differentially expressed miRNAs in exosomes derived from primary normal and ectopic endometrial cells. Methods We used miRNA microarray analysis to identify differentially expressed exosomal miRNAs. Among the selected exosomal miRNAs, we focused on hsa-miR-202-3p and hsa-miR-202-5p and validated their expression levels using quantitative reverse transcription polymerase chain reaction analysis. We then further examined their expression in exosomes derived from vaginal discharge (leukorrhea) from patients with EMS and the negative control group. Results The data show that hsa-miR-202-3p and hsa-miR-202-5p were expressed significantly higher in leukorrhea-derived exosomes from EMS patients compared with the negative controls. Conclusion Taken together, our results suggest that leukorrhea-derived exosomal hsa-miR-202 could serve as a potential useful biomarker for diagnosing EMS.

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Monastirioti, Alexia, Chara Papadaki, Konstantinos Rounis, Despoina Kalapanida, Dimitrios Mavroudis, and Sofia Agelaki. "A Prognostic Role for Circulating microRNAs Involved in Macrophage Polarization in Advanced Non-Small Cell Lung Cancer." Cells 10, no. 8 (August 5, 2021): 1988. http://dx.doi.org/10.3390/cells10081988.

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Circulating microRNAs (miRNAs) are key regulators of the crosstalk between tumor cells and immune response. In the present study, miRNAs (let-7c, miR-26a, miR-30d, miR-98, miR-195, miR-202) reported to be involved in the polarization of macrophages were examined for associations with the outcomes of non-small cell lung cancer (NSCLC) patients (N = 125) treated with first-line platinum-based chemotherapy. RT-qPCR was used to analyze miRNA expression levels in the plasma of patients prior to treatment. In our results, disease progression was correlated with high miR-202 expression (HR: 2.335; p = 0.040). Additionally, high miR-202 expression was characterized as an independent prognostic factor for shorter progression-free survival (PFS, HR: 1.564; p = 0.021) and overall survival (OS, HR: 1.558; p = 0.024). Moreover, high miR-202 independently predicted shorter OS (HR: 1.989; p = 0.008) in the non-squamous (non-SqCC) subgroup, and high miR-26a was correlated with shorter OS in the squamous (SqCC) subgroup (10.07 vs. 13.53 months, p = 0.033). The results of the present study propose that the expression levels of circulating miRNAs involved in macrophage polarization are correlated with survival measures in NSCLC patients, and their role as potential biomarkers merits further investigation.

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Jin, Yilin, Wei Liu, Yangxi Xiang, Wanwan Zhang, Hong Zhang, Kuntong Jia, and Meisheng Yi. "Maternal miR-202-5p is required for zebrafish primordial germ cell migration by protecting small GTPase Cdc42." Journal of Molecular Cell Biology 12, no. 7 (November 19, 2019): 530–42. http://dx.doi.org/10.1093/jmcb/mjz103.

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Abstract In many lower animals, germ cell formation, migration, and maintenance depend on maternally provided determinants in germ plasm. In zebrafish, these processes have been extensively studied in terms of RNA-binding proteins and other coding genes. The role of small non-coding RNAs in the regulation of primordial germ cell (PGC) development remains largely unknown and poorly investigated, even though growing interests for the importance of miRNAs involved in a wide variety of biological processes. Here, we reported the role and mechanism of the germ plasm-specific miRNA miR-202-5p in PGC migration: (i) both maternal loss and knockdown of miR-202-5p impaired PGC migration indicated by the mislocalization and reduced number of PGCs; (ii) cdc42se1 was a direct target gene of miR-202-5p, and overexpression of Cdc42se1 in PGCs caused PGC migration defects similar to those observed in loss of miR-202-5p mutants; (iii) Cdc42se1 not only interacted with Cdc42 but also inhibited cdc42 transcription, and overexpression of Cdc42 could rescue PGC migration defects in Cdc42se1 overexpressed embryos. Thus, miR-202-5p regulates PGC migration by directly targeting and repressing Cdc42se1 to protect the expression of Cdc42, which interacts with actin to direct PGC migration.

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Zhao, Wei, Youyang Wu, Fanhao Ye, Shiwei Huang, Hao Chen, Rui Zhou, and Wenbing Jiang. "Tetrandrine Ameliorates Myocardial Ischemia Reperfusion Injury through miR-202-5p/TRPV2." BioMed Research International 2021 (March 8, 2021): 1–16. http://dx.doi.org/10.1155/2021/8870674.

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Objective. This study is aimed at investigating the therapeutic effects of tetrandrine (Tet) on myocardial ischemia reperfusion (I/R) injury and probe into underlying molecular mechanism. Methods. H9C2 cells were divided into hypoxia/oxygenation (H/R) group, H/R+Tet group, H/R+Tet+negative control (NC) group, and H/R+Tet+miR-202-5p inhibitor group. RT-qPCR was utilized to monitor miR-202-5p and TRPV2 expression, and TRPV2 protein expression was detected via western blot and immunohistochemistry in H9C2 cells. Cardiomyocyte apoptosis was evaluated through detection of apoptosis-related markers and flow cytometry. Furthermore, myocardial enzyme levels were detected by ELISA. Rats were randomly separated into sham operation group, I/R group, I/R+Tet group (50 mg/kg), I/R+Tet+NC group, and I/R+Tet+miR-202-5p inhibitor group. miR-202-5p and TRPV2 mRNA expression was assessed by RT-qPCR. TRPV2 protein expression was detected through western blot and immunohistochemistry in myocardial tissues. Apoptotic levels were assessed via apoptosis-related proteins and TUNEL. Pathological changes were observed by H&E staining. Myocardial infarction size was examined by Evans blue-TCC staining. Results. Abnormally expressed miR-202-5p as well as TRPV2 was found in H/R H9C2 cells and myocardial tissues of I/R rats, which was ameliorated following Tet treatment. Tet treatment significantly suppressed H/R- or I/R-induced cardiomyocyte apoptosis. ELISA results showed that CK-MB and LDH levels were lowered by Tet treatment in H/R H9C2 cells and serum of I/R rats. H&E staining indicated that Tet reduced myocardial injury in I/R rats. Also, myocardial infarction size was lowered by Tet treatment. The treatment effects of Tet were altered following cotreatment with miR-202-5p inhibitor. Conclusion. Our findings revealed that Tet may ameliorate myocardial I/R damage via targeting the miR-202-5p/TRPV2 axis.

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Zhang, Jie, Xiao-Yan Li, Ping Hu, and Yuan-Sheng Ding. "lncRNA NORAD Contributes to Colorectal Cancer Progression by Inhibition of miR-202-5p." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 26, no. 9 (October 17, 2018): 1411–18. http://dx.doi.org/10.3727/096504018x15190844870055.

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Previous study indicates that long noncoding RNA NORAD could serve as a competing endogenous RNA to pancreatic cancer metastasis. However, its role in colorectal cancer (CRC) needs to be investigated. In the present study, we found that the expression of NORAD was significantly upregulated in CRC tissues. Furthermore, the expression of NORAD was positively related with CRC metastasis and patients’ poor prognosis. Knockdown of NORAD markedly inhibited CRC cell proliferation, migration, and invasion but induced cell apoptosis in vitro. In vivo experiments also indicated an inhibitory effect of NORAD on tumor growth. Mechanistically, we found that NORAD served as a competing endogenous RNA for miR-202-5p. We found that there was an inverse relationship between the expression of NORAD and miR-202-5p in CRC tissues. Moreover, overexpression of miR-202-5p in SW480 and HCT116 cells significantly inhibited cellular proliferation, migration, and invasion. Taken together, our study demonstrated that the NORAD/miR-202-5p axis plays a pivotal function on CRC progression.

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Xu, Wenjing, Liwei Xie, Yingying Yang, Jiayu Xu, Shang Cai, and Ye Tian. "KAT5 Inhibitor NU9056 Suppresses Anaplastic Thyroid Carcinoma Progression through c-Myc/miR-202 Pathway." International Journal of Endocrinology 2022 (February 11, 2022): 1–14. http://dx.doi.org/10.1155/2022/2014568.

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Background. Anaplastic thyroid carcinoma (ATC) is considered to be one of the most aggressive cancers. Our previous study proved that highly expressed lysine acetyltransferase 5 (KAT5) in ATC is associated with a poorer prognosis. Here, this study examined the effects of a KAT5 inhibitor (NU9056) in human ATC cells. Methods. First, the Cancer Genome Atlas (TCGA) dataset was used to detect the relationship between KAT5 expression and outcomes of thyroid carcinoma patients. Then, both in vitro and in vivo experiments were conducted to investigate the effects of NU9056 on normal and ATC human thyroid cells. Finally, microRNA sequencing, qPCR, and dual-luciferase reporter assay were performed to explore potential mechanisms by identifying downstream microRNA related to NU9056. Results. KAT5 dysregulation correlated with more advanced-stage and poorer outcomes of thyroid carcinoma patients. Endogenous KAT5 protein and mRNA levels were much higher in ATC cells than in normal thyroid cells. Suppression of KAT5 by NU9056 inhibited survival, growth, migration, invasion, and tube formation, and increased radiosensitivity and chemosensitivity in ATC cells but showed no impact on normal thyroid cells. Mechanistically, microRNA-202-5p (miR-202) was identified as the most significantly decreased miRNA after NU9056 treatment. Knockdown of miR-202 suppressed ATC cell progression, while forced expression of miR-202 partially blocked the inhibitory effect of NU9056 on ATC cells. Furthermore, c-Myc was validated as the transcription factor of miR-202, and NU9056 decreased the c-Myc protein level by shortening its half-life. Finally, we proved that NU9056 inhibited ATC proliferation in vivo. Conclusions. Our results indicated that NU9056 targets KAT5, shortens c-Myc half-life, subsequently downregulates miR-202 expression, and results in the suppression of ATC cells. Overall, KAT5 could be a potential target for clinical treatment for ATC.

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Marisaldi, Luca, Orsola Iorillo, Danilo Basili, Giorgia Gioacchini, Julien Bobe, Violette Thermes, Francesca Maradonna, and Oliana Carnevali. "A Comparison of Reproductive Performances in Young and Old Females: A Case Study on the Atlantic Bluefin Tuna in the Mediterranean Sea." Animals 11, no. 12 (November 23, 2021): 3340. http://dx.doi.org/10.3390/ani11123340.

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In the Mediterranean Sea, a demographic substructure of the Atlantic bluefin tuna Thunnus thynnus has emerged over the last decade, with old and young individuals exhibiting different horizontal movements and spatial–temporal patterns of gonad maturation. In the present study, histology and molecular reproductive markers were integrated with the gonad-specific mir-202 gene expression and ovarian localization to provide a comprehensive picture of the reproductive performances in young and old females and investigate the role played by the mir-202 during gonadal maturation. During the reproductive period, old females (>100 kg; 194.6 ± 33.9 cm straight fork length; 11.3 ± 2.7 years old) were found to have greater reproductive performances than younger females (<80 kg; 139.3 ± 18.8 cm straight fork length; 8.4 ± 1.1 years old) according to gene expression results, suggesting a prolonged spawning season, earlier arrival on spawning grounds and/or better condition in older females. The mir-202-5p showed no global changes; it was abundantly expressed in granulosa cells and faintly present in the ooplasm. On the other hand, the mir-202-3p expression profile reflected levels of oocyte maturation molecular markers (star, lhr) and both histological and molecular (casp3) levels of follicular atresia. Overall, old females exhibited greater reproductive performances than younger females, likely reflecting different reproductive dynamics linked to the physical condition, habitat usage and migratory behaviour. These results highlight the importance of preserving large and old females in the context of fishery management. Finally, the mir-202 appears to be a good candidate to regulate the reproductive output of this species in an autocrine/paracrine manner through either stage- or age-dependent processes.

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Sontakke, Sadanand D., Bushra T. Mohammed, Alan S. McNeilly, and F. Xavier Donadeu. "Characterization of microRNAs differentially expressed during bovine follicle development." REPRODUCTION 148, no. 3 (September 2014): 271–83. http://dx.doi.org/10.1530/rep-14-0140.

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Several different miRNAs have been proposed to regulate ovarian follicle function; however, very limited information exists on the spatiotemporal patterns of miRNA expression during follicle development. The objective of this study was to identify, using microarray, miRNA profiles associated with growth and regression of dominant-size follicles in the bovine monovular ovary and to characterize their spatiotemporal distribution during development. The follicles were collected from abattoir ovaries and classified as small (4–8 mm) or large (12–17 mm); the latter were further classified as healthy or atretic based on estradiol and CYP19A1 levels. Six pools of small follicles and individual large healthy (n=6) and large atretic (n=5) follicles were analyzed using Exiqon's miRCURY LNA microRNA Array 6th gen, followed by qPCR validation. A total of 17 and 57 sequences were differentially expressed (greater than or equal to twofold; P<0.05) between large healthy and each of small and large atretic follicles respectively. Bovine miRNAs confirmed to be upregulated in large healthy follicles relative to small follicles (bta-miR-144, bta-miR-202, bta-miR-451, bta-miR-652, and bta-miR-873) were further characterized. Three of these miRNAs (bta-miR-144, bta-miR-202, and bta-miR-873) were also downregulated in large atretic follicles relative to large healthy follicles. Within the follicle, these miRNAs were predominantly expressed in mural granulosa cells. Further, body-wide screening revealed that bta-miR-202, but not other miRNAs, was expressed exclusively in the gonads. Finally, a total of 1359 predicted targets of the five miRNAs enriched in large healthy follicles were identified, which mapped to signaling pathways involved in follicular cell proliferation, steroidogenesis, prevention of premature luteinization, and oocyte maturation.

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Donadeu, F. X., S. D. Sontakke, and J. Ioannidis. "MicroRNA indicators of follicular steroidogenesis." Reproduction, Fertility and Development 29, no. 5 (2017): 906. http://dx.doi.org/10.1071/rd15282.

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MicroRNAs (miRNAs) can provide useful biomarkers of tissue function. The aim of the present study was to determine, in bovine follicles (n = 66; diameter 4–22 mm), the relationship among several indices of steroidogenesis and levels of 15 miRNAs previously identified to be associated with follicle development. Oestradiol levels, the oestradiol : progesterone (E : P) ratio and cytochrome P450 family 19 subfamily A member 1 (CYP19A1) expression were strongly correlated with each other (ρ > 0.8) and with LH/choriogonadotropin receptor (LHCGR) expression (ρ ≥ 0.6; P < 0.01). Levels of nine different miRNAs in the follicular wall were correlated (P < 0.01) with oestradiol, the E : P ratio and CYP19A1, with miR-873 showing the strongest correlation in each case (ρ > 0.7). Analyses of follicular fluid miRNAs identified miR-202 as correlated with oestradiol, the E : P ratio and CYP19A1 (ρ > 0.5; P < 0.01). When considering all follicle end-points together, we found that using a cut-off value of E : P = 1 overestimated the number of oestrogen-inactive follicles, whereas using CYP19A1 as a classifier provided a clearer separation of follicle samples based on oestrogen activity, in agreement with the E : P ratio, LHCGR expression and levels of miR-873 and miR-202. In conclusion, we identified miR-873 and miR-202 as miRNAs whose levels in follicular tissues can be used as indicators of steroidogenic capacity in bovine. We showed that these or other gene expression parameters, in addition or alternatively to the E : P ratio, should be used to accurately classify follicles based on steroidogenic capacity.

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Su, Yan, Shiyou Lu, Jincun Li, and Liya Deng. "Shikonin-mediated up-regulation of miR-34a and miR-202 inhibits retinoblastoma proliferation." Toxicology Research 7, no. 5 (2018): 907–12. http://dx.doi.org/10.1039/c8tx00079d.

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Gay, Stéphanie, Jérôme Bugeon, Amine Bouchareb, Laure Henry, Clara Delahaye, Fabrice Legeai, Jérôme Montfort, et al. "MiR-202 controls female fecundity by regulating medaka oogenesis." PLOS Genetics 14, no. 9 (September 10, 2018): e1007593. http://dx.doi.org/10.1371/journal.pgen.1007593.

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Bizuayehu, Teshome Tilahun, and Igor Babiak. "Heterogenic Origin of Micro RNAs in Atlantic Salmon (Salmo salar) Seminal Plasma." International Journal of Molecular Sciences 21, no. 8 (April 15, 2020): 2723. http://dx.doi.org/10.3390/ijms21082723.

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The origin and contribution of seminal plasma RNAs into the whole semen RNA repertoire are poorly known, frequently being overlooked or neglected. In this study, we used high-throughput sequencing and RT-qPCR to profile microRNA (miRNA) constituents in the whole semen, as well as in fractionated spermatozoa and seminal plasma of Atlantic salmon (Salmo salar). We found 85 differentially accumulated miRNAs between spermatozoa and the seminal plasma. We identified a number of seminal plasma-enriched and spermatozoa-enriched miRNAs. We localized the expression of some miRNAs in juvenile and mature testes. Two abundant miRNAs, miR-92a-3p and miR-202-5p, localized to both spermatogonia and somatic supporting cells in immature testis, and they were also highly abundant in somatic cells in mature testis. miR-15c-5p, miR-30d-5p, miR-93a-5p, and miR-730-5p were detected only in mature testis. miRs 92a-3p, 202-5p, 15c-5p, and 30d-5p were also detected in a juvenile ovary. The RT-qPCR experiment demonstrated lack of correlation in miRNA transcript levels in seminal plasma versus blood plasma. Our results indicate that salmon semen is rich in miRNAs, which are present in both spermatozoa and seminal plasma. Testicular-supporting somatic cells are likely the source of seminal plasma enrichment, whereas blood plasma is unlikely to contribute to the seminal plasma miRNA repertoire.

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Lagah, S., T. J. Sood, P. Palta, M. Mukesh, R. S. Manik, M. Chauhan, and S. K. Singla. "32 NEXT-GENERATION SEQUENCING DISCLOSES DIFFERENCES IN microRNA EXPRESSION PROFILES OF BUFFALO (BUBALUS BUBALIS) EMBRYOS PRODUCED BY HAND-MADE CLONING AND IN VITRO FERTILIZATION." Reproduction, Fertility and Development 29, no. 1 (2017): 123. http://dx.doi.org/10.1071/rdv29n1ab32.

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Mammalian embryo development is a complex process with a series of critical events taking place at every stage of development. It is an established fact that the birth rate of animals produced by nuclear transfer (NT) is far less (<2%) than that of IVF embryos (40%) after successful embryo transfers in different farm animal species. Micro(mi)RNAs are small non-coding RNAs of 17 to 25 nucleotides that alter the function of their target genes by either degrading them or inhibiting their expression. MiRNAs play a vital role during mammalian embryo development and may be adding to the extremely low birth rate and abnormalities in cloned animals. The present study was done with an objective of comparing the miRNA expression profiles of pre-implantation buffalo blastocysts produced by handmade cloning (HMC) and IVF. We hypothesised that there may be differences in the profiles of miRNAs expressed between the 2 groups that contribute to higher success rate in IVF group compared with HMC. Next-generation sequencing (NGS) was done to generate and compare the miRNA profiles and further discern the differentially expressed miRNAs between the 2 groups of blastocysts. For this study, NT blastocysts were produced using fibroblast donor cells isolated from ear skin of a buffalo bull. To produce genetically half-identical IVF blastocysts, the semen of the same bull was used. The oocytes used for generation of both HMC and IVF blastocysts were aspirated from buffalo ovaries obtained from abattoir. Total RNA was isolated from HMC and IVF blastocysts in 4 pools of each group. Each pool consisted of 40 blastocysts. A MiRNA cDNA library was prepared which was then subjected to NGS on Illumina HiSEqn 2000 (Illumina Inc., San Diego, CA, USA). Bos taurus genome was taken as reference to align the reads generated. The data from NGS was validated by RT-qPCR, taking 10 miRNAs (mir-15a, mir-23a, mir-128, mir-130a, mir-133a, mir-194, mir-196b, mir-200b, mir-431 and mir-451). The results positively validated the NGS data. Differential expression analysis of miRNAs between the 2 types of blastocysts revealed that the number of differentially expressed miRNAs with fold change of ≥ 2.0 were 74, with 52 miRNAs up-regulated in HMC and 22 miRNAs up-regulated in IVF. At significance level of P < 0.2, there were 2 miRNAs (mir-202 and mir-133a) that were uniquely expressed in IVF blastocysts and 8 miRNAs (mir-219, mir-451, mir-497, mir-33a, mir-2448, mir-592, mir-187, and mir-502a) that were uniquely expressed in HMC blastocysts. According to the gene ontology analysis, mir-202 is involved in negative regulation of apoptosis and positive regulator of cell growth, whereas mir-133a is involved in generating immunity. Absence of mir-202 and mir-133a expression from HMC blastocysts may be contributing to high apoptosis and other abnormalities in them compared with IVF counterparts. The NGS results indicate that the miRNA profiles of HMC and IVF blastocysts show huge differences. Further analysis of these differentially expressed miRNAs may open the door to miRNA therapies for treating the HMC blastocysts by regulating the expression of critical miRNAs in HMC blastocysts, thereby improving the success rate of cloning.

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Schaefer, Jeremy, Niyati Nakra, Dina Montufar-Solis, Nadarajah Vigneswaran, and John Klein. "P-202 IL-10 Mediated Regulation of miR-223 and Roquin." Inflammatory Bowel Diseases 19 (December 2013): S106. http://dx.doi.org/10.1097/01.mib.0000439001.00060.21.

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Lee, Soon-Tae, Kon Chu, Keun-Hwa Jung, Jae-Jun Ban, Woo-Seok Im, Hee-Yeon Jo, Ji-Hyun Park, et al. "Altered Expression of miR-202 in Cerebellum of Multiple-System Atrophy." Molecular Neurobiology 51, no. 1 (July 1, 2014): 180–86. http://dx.doi.org/10.1007/s12035-014-8788-4.

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Fang, Baojun, Limin Wei, Kejun Dong, Xiaohui Niu, Xiuhui Sui, and Hongquan Zhang. "miR‐202 modulates the progression of neuropathic pain through targeting RAP1A." Journal of Cellular Biochemistry 120, no. 3 (December 5, 2018): 2973–82. http://dx.doi.org/10.1002/jcb.27025.

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Czop, Marcin, Karolina Gasińska, Ewa Kosior-Jarecka, Dominika Wróbel-Dudzińska, Janusz Kocki, and Tomasz Żarnowski. "Twenty Novel MicroRNAs in the Aqueous Humor of Pseudoexfoliation Glaucoma Patients." Cells 12, no. 5 (February 24, 2023): 737. http://dx.doi.org/10.3390/cells12050737.

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The microRNAs (miRNAs) are short non-coding RNAs (19–25 nt) that regulate the level of gene expression at the post-transcriptional stage. Altered miRNAs expression can lead to the development of various diseases, e.g., pseudoexfoliation glaucoma (PEXG). In this study, we assessed the levels of miRNA expression in the aqueous humor of PEXG patients using the expression microarray method. Twenty new miRNA molecules have been selected as having the potential to be associated with the development or progression of PEXG. Ten miRNAs were downregulated in PEXG (hsa-miR-95-5p, hsa-miR-515-3p, hsa-mir-802, hsa-miR-1205, hsa-miR-3660, hsa-mir-3683, hsa -mir-3936, hsa-miR-4774-5p, hsa-miR-6509-3p, hsa-miR-7843-3p) and ten miRNAs were upregulated in PEXG (hsa-miR-202 -3p, hsa-miR-3622a-3p, hsa-mir-4329, hsa-miR-4524a-3p, hsa-miR-4655-5p, hsa-mir-6071, hsa-mir-6723-5p, hsa-miR-6847-5p, hsa-miR-8074, and hsa-miR-8083). Functional analysis and enrichment analysis showed that the mechanisms that can be regulated by these miRNAs are: extracellular matrix (ECM) imbalance, cell apoptosis (possibly retinal ganglion cells (RGCs)), autophagy, and elevated calcium cation levels. Nevertheless, the exact molecular basis of PEXG is unknown and further research is required on this topic.

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Li, Wenjun, Xuechao Xu, Yixin Wan, Hong Wang, Hongyan Tao, and Huirong Huang. "Cynaropicrin inhibits lung cancer proliferation by targeting EGFR/AKT signaling pathway." Tropical Journal of Pharmaceutical Research 20, no. 4 (January 20, 2022): 715–20. http://dx.doi.org/10.4314/tjpr.v20i4.8.

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Purpose: To investigate the anti-proliferative effect of cynaropicrin on lung cancer cell lines, and the underlying molecular mechanism. Methods: The effect of cynaropicrin treatment on the viabilities of H1975 and H460 cells was measured using Cell Counting Kit-8. Apoptosis was analysed by annexin-V/FITC staining, while protein expressions were assayed by western blotting. Results: Treatment of H1975 and H460 cells with cynaropicrin at doses of 0.25 – 2.0 μM led to a marked reduction in their viability (p < 0.05). In cynaropicrin-treated H1975 and H460 cells, there was significant increase in apoptosis, when compared to control cells. Caspase-3 and caspase-9 levels were also significantly increased in H1975 and H460 cells on treatment with cynaropicrin at doses of 0.25 and 2.0 μM while treatment with cynaropicrin at doses of 0.25 - 2.0 μM significantly down-regulated the mRNA expression of CCND1 in the two cell lines (p < 0.05). Cynaropicrin markedly inhibited mRNA and protein expressions of EGFR, and also downregulated AKT in H1975 and H460 cells (p < 0.05). However, cynaropicrin significantly increased the expressions of miR-202 and miR-370. Conclusion: Cynaropicrin exerts anti-proliferative and proapoptotic effects on H1975 and H460 lung cancer cells via deactivation of EGFR/AKT signaling pathway. Moreover, it upregulated the expressions of miR-202 and miR-370 in these cells. Thus, cynaropicrin has potentials for the treatment of lung cancer.

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Li, Jin, Baohua Zhang, Qihuang Chen, and Qiang Li. "miR-202 Mediates Metabolic Shift in Lung Cancer Cells via Targeting HK2." Current Signal Transduction Therapy 9, no. 2 (February 12, 2015): 101–5. http://dx.doi.org/10.2174/1574362410666150107234535.

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Wang, Li, Xueyan Liu, Xicheng Song, Lei Dong, and Dawei Liu. "MiR-202-5p Promotes M2 Polarization in Allergic Rhinitis by Targeting MATN2." International Archives of Allergy and Immunology 178, no. 2 (November 8, 2018): 119–27. http://dx.doi.org/10.1159/000493803.

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Li, Shizhu, Genmei Lin, Wenyu Fang, Dong Gao, Jing Huang, Jingui Xie, and Jianguo Lu. "Identification and Comparison of microRNAs in the Gonad of the Yellowfin Seabream (Acanthopagrus Latus)." International Journal of Molecular Sciences 21, no. 16 (August 8, 2020): 5690. http://dx.doi.org/10.3390/ijms21165690.

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Yellowfin seabream (Acanthopagrus latus) is a commercially important fish in Asian coastal waters. Although natural sex reversal has been described in yellowfin seabream, the mechanisms underlying sexual differentiation and gonadal development in this species remain unclear. MicroRNAs (miRNAs) have been shown to play crucial roles in gametogenesis and gonadal development. Here, two libraries of small RNAs, constructed from the testes and ovaries of yellowfin seabream, were sequenced. Across both gonads, we identified 324 conserved miRNAs and 92 novel miRNAs: 67 ovary-biased miRNAs, including the miR-200 families, the miR-29 families, miR-21, and miR-725; and 88 testis-biased miRNAs, including the let-7 families, the miR-10 families, miR-7, miR-9, and miR-202-3p. GO (Gene Ontology) annotations and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analyses of putative target genes indicated that many target genes were significantly enriched in the steroid biosynthesis pathway and in the reproductive process. Our integrated miRNA-mRNA analysis demonstrated a putative negatively correlated expression pattern in yellowfin seabream gonads. This study profiled the expression patterns of sex-biased miRNAs in yellowfin seabream gonads, and provided important molecular resources that will help to clarify the miRNA-mediated post-transcriptional regulation of sexual differentiation and gonadal development in this species.

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Shang, Zhiwei, and Hongwen Li. "Altered expression of four miRNA (miR-1238-3p, miR-202-3p, miR-630 and miR-766-3p) and their potential targets in peripheral blood from vitiligo patients." Journal of Dermatology 44, no. 10 (May 13, 2017): 1138–44. http://dx.doi.org/10.1111/1346-8138.13886.

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Santos, Nathalia L., Silvina O. Bustos, Patricia P. Reis, Roger Chammas, and Luciana N. S. Andrade. "Extracellular Vesicle-Packaged miR-195-5p Sensitizes Melanoma to Targeted Therapy with Kinase Inhibitors." Cells 12, no. 9 (May 5, 2023): 1317. http://dx.doi.org/10.3390/cells12091317.

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Management of advanced melanoma remains challenging, with most BRAF (B-Raf proto-oncogene, serine/threonine kinase)-mutated metastatic patients relapsing within a few months upon MAPK inhibitors treatment. Modulation of tumor-derived extracellular vesicle (EVs) cargo with enrichment of antitumoral molecules is a promising strategy to impair tumor progression and increase treatment response. Herein, we report that restored expression of miR-195-5p, down-regulated in melanoma favoring drug resistance, increases the release of EVs enriched in the tumor suppressor miRNAs, miR-195-5p, miR-152-3p, and miR-202-3p. Incorporating these EVs by bystander tumor cells resulted in decreased proliferation and viability, accompanied by a reduction in CCND1 and YAP1 mRNA levels. Upon treatment with MAPK inhibitors, miR-195 EVs significantly decreased BCL2-L1 protein levels and increased cell death ratio and treatment efficacy. Additionally, EVs exogenously loaded with miR-195-5p by electroporation reduced tumor volume in vivo and impaired engraftment and growth of xenografts implanted with melanoma cells exposed to MAPK inhibitors. Our study shows that miR-195-5p antitumoral activity can be spread to bystander cells through EVs, improving melanoma response to targeted therapy and revealing a promising EV-based strategy to increase clinical response in patients harboring BRAF mutations.

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Poel, Boyd, Beekhof, Schelfhorst, Pham, Piersma, Knol, Jimenez, Verheul, and Buffart. "Proteomic Analysis of miR-195 and miR-497 Replacement Reveals Potential Candidates that Increase Sensitivity to Oxaliplatin in MSI/P53wt Colorectal Cancer Cells." Cells 8, no. 9 (September 19, 2019): 1111. http://dx.doi.org/10.3390/cells8091111.

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Most patients with advanced colorectal cancer (CRC) eventually develop resistance to systemic combination therapy. miR-195-5p and miR-497-5p are downregulated in CRC tissues and associated with drug resistance. Sensitization to 5-FU, oxaliplatin, and irinotecan by transfection with miR-195-5p and miR-497-5p mimics was studied using cell viability and clonogenic assays in cell lines HCT116, RKO, DLD-1, and SW480. In addition, proteomic analysis of transfected cells was implemented to identify potential targets. Significantly altered proteins were subjected to STRING (protein-protein interaction networks) database analysis to study the potential mechanisms of drug resistance. Cell viability analysis of transfected cells revealed increased sensitivity to oxaliplatin in microsatellite instable (MSI)/P53 wild-type HCT116 and RKO cells. HCT116 transfected cells formed significantly fewer colonies when treated with oxaliplatin. In sensitized cells, proteomic analysis showed 158 and 202 proteins with significantly altered expression after transfection with miR-195-5p and miR-497-5p mimics respectively, of which CHUK and LUZP1 proved to be coinciding downregulated proteins. Resistance mechanisms of these proteins may be associated with nuclear factor kappa-B signaling and G1 cell-cycle arrest. In conclusion, miR-195-5p and miR-497-5p replacement enhanced sensitivity to oxaliplatin in treatment naïve MSI/P53 wild-type CRC cells. Proteomic analysis revealed potential miRNA targets associated with the cell-cycle which possibly bare a relation with chemotherapy sensitivity.

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Meng, Xiangrui, Xiaoqi Chen, Peng Lu, Wang Ma, Dongli Yue, Lijie Song, and Qingxia Fan. "miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 25, no. 2 (January 26, 2017): 215–23. http://dx.doi.org/10.3727/096504016x14732772150541.

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Hoffman, Aaron E., Ran Liu, Alan Fu, Tongzhang Zheng, Frank Slack, and Yong Zhu. "Targetome Profiling, Pathway Analysis and Genetic Association Study Implicate miR-202 in Lymphomagenesis." Cancer Epidemiology Biomarkers & Prevention 22, no. 3 (January 18, 2013): 327–36. http://dx.doi.org/10.1158/1055-9965.epi-12-1131-t.

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Zhao, Yu, Chenglong Li, Ming Wang, Liping Su, Ying Qu, Jianfang Li, Beiqin Yu, et al. "Decrease of miR-202-3p Expression, a Novel Tumor Suppressor, in Gastric Cancer." PLoS ONE 8, no. 7 (July 25, 2013): e69756. http://dx.doi.org/10.1371/journal.pone.0069756.

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Lin, Yilin, Zhihua Chen, Suyong Lin, Yan Zheng, Yisu Liu, Ji Gao, and Shaoqin Chen. "MiR-202 inhibits the proliferation and invasion of colorectal cancer by targeting UHRF1." Acta Biochimica et Biophysica Sinica 51, no. 12 (August 8, 2019): 1305–6. http://dx.doi.org/10.1093/abbs/gmz088.

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Amini Khorasgani, Majid, Parisa Mohammady Nejad, and Mohammad Mehdi Moghani Bashi. "Increased Expression of miR-202-3p in Patients with Relapsing-Remitting Multiple Sclerosis." Jorjani Biomedicine Journal 6, no. 4 (December 1, 2018): 8–18. http://dx.doi.org/10.29252/jorjanibiomedj.6.4.8.

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Mody, Hardik R., Sau Wai Hung, Rakesh K. Pathak, Jazmine Griffin, Zobeida Cruz-Monserrate, and Rajgopal Govindarajan. "miR-202 Diminishes TGFβ Receptors and Attenuates TGFβ1-Induced EMT in Pancreatic Cancer." Molecular Cancer Research 15, no. 8 (April 3, 2017): 1029–39. http://dx.doi.org/10.1158/1541-7786.mcr-16-0327.

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Sun, Zhengwen, Tongqing Zhang, Huanyu Hong, Qingxia Liu, and Haiguang Zhang. "miR-202 suppresses proliferation and induces apoptosis of osteosarcoma cells by downregulating Gli2." Molecular and Cellular Biochemistry 397, no. 1-2 (August 26, 2014): 277–83. http://dx.doi.org/10.1007/s11010-014-2195-z.

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Huang, Zong-Sheng, Xian-Wen Guo, Guo Zhang, Lie-Xin Liang, and Bing Nong. "The Diagnostic and Prognostic Value of miR-200c in Gastric Cancer: A Meta-Analysis." Disease Markers 2019 (April 4, 2019): 1–9. http://dx.doi.org/10.1155/2019/8949618.

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Background. The role of miR-200c in gastric cancer remains controversial. This study is aimed at clarifying the diagnostic and prognostic value of miR-200c in gastric cancer through a meta-analysis. Methods. A comprehensive literature search of PubMed, Embase, and Ovid library databases was conducted. The studies included were those conducted before December 2017. The sensitivity and specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and area under curve (AUC) were used to estimate the diagnostic value of miR-200c. Meanwhile, the pooled hazard ratio (HR) was used to estimate the prognostic value of miR-200c. Results. For the diagnostic value of miR-200c, six studies that included 202 patients with gastric cancer and 250 normal controls were analyzed. The sensitivity, specificity, PLR, NLR, DOR, and AUC were 0.74, 0.66, 2.20, 0.40, 5.34, and 0.75, respectively. Subgroup analysis showed no significant difference in the type of the sample, method for testing miR-200c, and ethnicity among the patients. Meanwhile, for the prognostic value of miR-200c, seven studies comprising 935 patients with gastric cancer were analyzed. The pooled results showed that miR-200c expression was associated with overall survival (HR=2.19) and disease-free survival (HR=1.73), but not with progression-free survival (HR=1.64) in patients with gastric cancer. There was no publication bias across the studies. Conclusions. Both serum and tissue miR-200c have moderate diagnostic accuracy in gastric cancer. miR-200c could also be used as a valuable indicator for predicting the prognosis of gastric cancer patients.

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Raveche, Elizabeth S., Erica Salerno, Brian J. Scaglione, Vijaya Manohar, Fatima Abbasi, Yi-Chu Lin, Torgny Fredrickson, et al. "Abnormal microRNA-16 locus with synteny to human 13q14 linked to CLL in NZB mice." Blood 109, no. 12 (June 15, 2007): 5079–86. http://dx.doi.org/10.1182/blood-2007-02-071225.

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Abstract New Zealand black (NZB) mice with autoimmune and B lymphoproliferative disease (B-LPD) are a model for human chronic lymphocytic leukemia (CLL). A genomewide linkage scan of the NZB loci associated with lymphoma was conducted in F1 backcrosses of NZB and a control strain, DBA/2. Of 202 mice phenotyped for the presence or absence of LPD, surface maker expression, DNA content, and microsatellite polymorphisms, 74 had disease. The CD5+, IgM+, B220dim, hyperdiploid LPD was linked to 3 loci on chromosomes 14, 18, and 19 that are distinct from previously identified autoimmunity-associated loci. The region of synteny with mouse D14mit160 is the human 13q14 region, associated with human CLL, containing microRNAs mir-15a16-1. DNA sequencing of multiple NZB tissues identified a point mutation in the 3′ flanking sequence of the identical microRNA, mir-16-1, and this mutation was not present in other strains, including the nearest neighbor, NZW. Levels of miR-16 were decreased in NZB lymphoid tissue. Exogenous miR-16 delivered to an NZB malignant B-1 cell line resulted in cell-cycle alterations and increased apoptosis. Linkage of the mir-15a/16-1 complex and the development of B-LPD in this spontaneous mouse model suggest that the altered expression of the mir-15a/16-1 is the molecular lesion in CLL.

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Dou, Dou, Yan-Fen Shi, Qing Liu, Jie Luo, Ji-Xi Liu, Meng Liu, Ying-Ying Liu, Yuan-Liang Li, Xu-Dong Qiu, and Huang-Ying Tan. "Hsa-miR-202-3p, up-regulated in type 1 gastric neuroendocrine neoplasms, may targetDUSP1." World Journal of Gastroenterology 24, no. 5 (February 7, 2018): 573–82. http://dx.doi.org/10.3748/wjg.v24.i5.573.

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Journal articles on the topic 'MiR-202'

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