ArticleOncoTargets and therapy2019
MicroRNA-562 negatively regulated c-MET/AKT pathway in the growth of glioblastoma cells.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Hsa_circ_0093741 competes with FRS2 for miR-562 binding sites to promote nephroblastoma progression.Histology and histopathology · 2023Article
- The Role of Micro RNAs in Regulating PI3K/AKT Signaling Pathways in Glioblastoma.Iranian journal of pathology · 2022Review
- The Role of MiRNA in Cancer: Pathogenesis, Diagnosis, and Treatment.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Genomic alterations associated with mutational signatures, DNA damage repair and chromatin remodeling pathways in cervical carcinoma.NPJ genomic medicine · 2021Article
- Prognostic value of microRNA-378 in esophageal cancer and its regulatory effect on tumor progression.Experimental and therapeutic medicine · 2021Article
- Immune Modulatory Short Noncoding RNAs Targeting the Glioblastoma Microenvironment.Frontiers in oncology · 2021Review
- MiR-920 and LSP1 co-regulate the growth and migration of glioblastoma cells by modulation of JAK2/STAT5 pathway.Journal of bioenergetics and biomembranes · 2020Article
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6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNA-562 (miR-562) has been found to possess anti-cancer function in certain tumors. However, the function of miR-562 in glioblastoma (GBM) is still not fully understood. PURPOSE: The aim at present study is to analyze the function of miR-562 and its possible target in GBM cells. PATIENTS AND
methodsIn the present study, a total of 80 GBM samples and 16 adjacent noncancerous tissues were used to examine the expression of miR-562 and c-MET. In order to gain a deep insight into the molecular network of miR-562 and c-MET in GBM, the miR-562 mimic and inhibitor were transfected into two GBM cell lines (U251 and U87), respectively. Meanwhile, lentiviral vector was used to mediate overexpression of c-MET. Cell proliferation was examined via Cell Counting Kit-8 (CCK-8) assays. Meanwhile, cell apoptosis was analyzed by Annexin V-FTTC/PI staining assay.
resultsOur results indicated that the level of miR-562 was downregulated in GBM tissues and the expression of c-MET was upregulated in tumors. Cell proliferation analysis indicated that miR-562 was an anti-proliferation effector in GBM cells. Moreover, cell apoptosis analysis suggested the pro-apoptosis function of miR-562 in GBM cells.
conclusionOur results demonstrated that miR-562 negatively regulated the c-MET/AKT signal pathway. In addition, caspase-3 might also serve as another target for miR-562 in GBM cells. This research not only obtained a deep understanding of miR-562 but also provided evidence in terms of developing new prognostic biomarker for GBM.
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