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MiR-125b acts as an oncogene in glioblastoma cells and inhibits cell apoptosis through p53 and p38MAPK-independent pathways

文献类型： 外文期刊

作者： Wu, N. 1 ; Lin, X. 2 ; Zhao, X. 3 ; Zheng, L. 4 ; Xiao, L. 1 ; Liu, J. 1 ; Ge, L. 1 ; Cao, S. 6 ;

作者机构： 1.Chinese Acad Sci, Inst Oceanol, Qingdao 266071, Peoples R China

2.Capital Med Univ, Dept Pharmacol, Beijing 100069, Peoples R China

3.Qingdao Univ, Cent Lab, Affiliated Hosp, Coll Med, Qingdao 266003, Peoples R China

4.Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, Qingdao 266071, Peoples R China

5.Qingdao Agr Univ, Coll Chem & Pharmaceut Sci, Qingdao 266109, Peoples R China

6.Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA

期刊名称：BRITISH JOURNAL OF CANCER （ 影响因子：7.64； 五年影响因子：7.57 ）

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收录情况： SCI

摘要： Background: We have recently identified miR-125b upregulation in glioblastoma (GMB). The aim of this study is to determine the correlation between miR-125b expression and malignant grades of glioma and the genes targeted by miR-125b. Methods: Real-time PCR was employed to measure the expression level of miR-125b. Cell viability was evaluated by cell growth and colony formation in soft-agar assays. Cell apoptosis was determined by Hoechst 33342 staining and AnnexinV-FITC assay. The Luciferase assay was used to confirm the actual binding sites of p38MAPK mRNA. Western blot was used to detect the gene expression level. Results: The expression level of miR-125b is positively correlated with the malignant grade of glioma. Ectopic expression of miR-125b promotes the proliferation of GMB cells. Knockdown of endogenous miR-125b inhibits cell proliferation and promotes cell apoptosis. Further studies reveal that p53 is regulated by miR-125b. However, downregulation of the endogenous miR-125b also results in p53-independent apoptotic pathway leading to apoptosis in p53 mutated U251 cells and p53 knockdown U87 cells. Moreover, p38MAPK is also regulated by miR-125b and downregulation of miR-125b activates the p38MAPK-induced mitochondria apoptotic pathway. Conclusion: High-level expression of miR-125b is associated with poor outcomes of GMB. MiR-125b may have an oncogenic role in GMB cells by promoting cell proliferation and inhibiting apoptosis.

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