cerebral ischemia is a common cerebrovascular disease caused by the occlusion of a cerebral blood vessel. Micrornas (mirnas/mirs) are emerging regulators of various human diseases, including cerebral ischemia. upregulation of mir-183-5p has been reported to alleviate liver injury induced by ischemia-reperfusion (i/r). However, the effect of mir-183-5p on cerebral ischemia injury remains unknown. The present study evaluated the effects of mir-183-5p on ischemia injury using ischemic models of mouse brains exposed to transient middle cerebral artery occlusion and neuro-2a (n2a) neuroblastoma cells exposed to oxygen-glucose-deprivation (oGd) and subsequently reoxygenated. ischemia was evaluated in mice using neurological function scores, cerebral edema, 2,3,5-triphenyltetrazoliumchloride, nissl and Fluoro-Jade B staining assays. in addition, mir-183-5p expression, n2a cell viability and the expression levels of apoptosis-associated proteins were detected by quantitative Pcr, cell counting Kit-8 assay, flow cytometry and western blotting. The association between mir-183-5p and phosphatase and tensin homolog (PTEN) was also confirmed by a luciferase reporter assay. The results revealed that mir-183-5p expression was decreased and brain damage was increased in ischemic mice compared with the sham group. additionally, mir-183-5p levels were reduced, and apoptosis was increased in n2a cells exposed to ischemia compared with the control group. Following transfection with agomir-183-5p, cerebral ischemic injury and apoptosis levels were reduced in the in vivo i/r stroke model and oGd-induced n2a cells. in addition, PTen was determined to be a target of mir-183-5p following elucidation of a direct binding site. overexpression of PTen reversed the mir-183-5p-induced n2a cell apoptosis inhibition and survival after oGd. The results of the present study suggested that mir-183-5p reduced ischemic injury by negatively regulating PTen, which may aid the development of a novel therapeutic strategy for cerebral ischemia.
In recent years, the incidence of neuroglioma (glioma) has trended towards a younger age-group. Gene therapy has been widely implemented and a growing number of microRNAs associated with glioma have been identified., Herein, we detected the expression of micro RNA - miR-133b - in glioma by qPCR and also its effect on cell viability, survival and apoptosis of in vitro U87 and A172 cells. The binding effect of miR-133b on epithelial membrane protein-2 (EMP2) was verified and we then investigated the effect of EMP2 on in vitro glioma cells and tested the expression of apoptosis related factors after administration of altered miR-133b and EMP2 expressions. We found that miR-133b was down-regulated in glioma compared to adjacent non-tumorous tissue and also that its over-expression inhibits cell viability and survival and enhances apoptosis in the U87 and A-172 cells. Moreover, miR-133b effectively binds to EMP2, down-regulates its expression and negates its normal function. EMP2 normally promotes cell apoptosis and reduces cell viability and survival while miR-133b over-expression regulates the expression of apoptotic-associated protein and activates the apoptotic pathway, thus counteracting EMP2 regulation of opposite expression effects. Further, miR-133b can be considered a tumor suppressor because of its low expression and effects on cell apoptosis via down-regulating EMP2 expression and activating the apoptotic cell pathway in glioma. EMP2 is a risk factor for glioma, and miR-133b should prove a potential target for glioma clinical prevention and treatment.
Aim/Background: Glioma is a malignant brain tumor with the characteristics of rapid growth, diffuse invasion and therapeutic resistance. MicroRNAs (miRNAs) recently have be studied for the treatment of glioma. Here, we conducted cell-based experiments to analyze the role of miR-425-5p by targeting RAB2B in glioma though regulating the proliferation, invasion and migration of glioma cells. Methods: The qRT-PCR analysis detected the expression level of miR-425-5p in glioma cells. The transfection efficiency was verified by qRT-PCR. Cell viability, cell apoptosis, and the expression of cell cycle regulators were determined by CCK-8, flow cytometry and western blot analysis, respectively. And, the invasion and migration of glioma cells were assessed by wound-healing experiment and transwell assay. Result: Among five kinds of human glioma cell lines (U251, SHG44, LN229, T98G), the U251 cell line was chosen for the subsequent experiment. MiR-425-5p overexpression inhibited the proliferation, invasion and migration of glioma cells and promoted the glioma cells apoptosis. In addition, RAB2B was demonstrated to be a target of miR-129-5p. RAB2B inhibition could also inhibited the proliferation, invasion and migration of glioma cells and promoted the glioma cells apoptosis. Conclusion: Our findings suggested that miR-425-5p could inhibit the proliferation, invasion and migration, and promoted apoptosis of glioma cells by downregulation of RAB2B.
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