胶质瘤中 HuR 通过上调 PTBP1 表达激活 Akt 通路 对胶质瘤细胞的作用研究.

Objective To investigate the role of human antigen R (HuR) in glioma and its possible mechanism. Methods 21 cases of glioma tissue and normal control tissue were collected. Normal glioma cell line SVGp12 and human glioblastoma-derived cell line U251 were cultured in vitro, qRT-PCR was used to detect the mRNA expression of HuR and polypyrimidine tract-binding protein 1 (PTBP1) in tissues and cells. Western Blot was used to detect the protein expression of HuR, PTBP1, phosphorylated protein kinase B(p-Akt) and protein kinase B (Akt) in tissues and cells. RNA-binding protein immunoprecipitation test was used to detect the regulatory effect of HuR on PTBP1. CCK-8 was used to detect cell viability. EdU test was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. Results Compared with the normal control group, the mRNA and protein expression of HuR, and the mRNA and protein expression of PTBP1 in the glioma group were significantly increased (all P < 0. 05). Compared with the SVGp12 group, the mRNA and protein expression of HuR, and the mRNA and protein expression of PTBP1 in the U251 group were significantly increased (all P < 0. 05). HuR regulated the expression of PTBP1 by binding to PTBP1 mRNA. There was no statistically significant difference in the indicators between the blank group and the si-NC + oe-NC group (all P > 0. 05). Compared with the si-NC + oe-NC group, the mRNA and protein expressions of HuR and PTBP1 in the si-HuR group + oe-NC group were significantly reduced (all P < 0. 05), and the cell viability at 48 h and 72 h and the proliferation ability of cell were significantly reduced (all P < 0. 05), cell apoptosis was significantly increased (P < 0. 05), and the protein expression of p-Akt/Akt was significantly reduced (P < 0. 05). Compared with the si-HuR + oe-NC group, the mRNA and protein expression of HuR in the cells of the si-HuR + oe-PTBP1 group was not statistically different (all P > 0. 05), while the expression of PTBP1 mRNA and protein was significantly increased (all P < 0. 05), cell viability at 48 h and 72 h and the proliferation ability of cell were significantly increased (all P < 0. 05). Cell apoptosis was significantly reduced (P < 0. 05), and the protein expression of p-Akt/Akt was significantly increased (P < 0. 05). Conclusion HuR may activate Akt pathway by up-regulating the expression of PTBP1 to promote the proliferation of glioma cells and inhibit cell apoptosis. [ABSTRACT FROM AUTHOR]