Curcumin affects autophagy of prolactinoma cells by upregulating miR‐206 to exert antitumor effects

姜黄素 PI3K/AKT/mTOR通路 蛋白激酶B 自噬 基因敲除 下调和上调 化学 细胞生长 活力测定 癌症研究 免疫印迹 信号转导 细胞生物学 细胞 分子生物学 生物 细胞凋亡 生物化学 基因
作者
Jia‐feng Duan,Qiujuan Zhang,Jin Zhu,Jia‐hui Lu
出处
期刊:Journal of Biochemical and Molecular Toxicology [Wiley]
卷期号:38 (6) 被引量:1
标识
DOI:10.1002/jbt.23734
摘要

We explored the effects of curcumin on the aberrant biological behaviors of prolactinoma cells and the downstream pathways through which curcumin exerts its antitumor effects. We used quantitative reverse transcription-polymerase chain reaction assays to measure miR-206 expression levels in peripheral blood samples from patients with prolactinoma before and after curcumin treatment. We also investigated the proliferation level, viability, and invasion ability of groups of cells treated with different concentrations of curcumin using 3-(4,5)-dimethylthiahiazo (-z-y1)-3-di-phenytetrazoliumromide (MTT) assays, cell cloning assays, and Transwell assays, respectively. Furthermore, we determined the levels of autophagy-related proteins and protein kinase B/mammalian target of the rapamycin (Akt/mTOR) signaling pathway-related proteins in each group of treated cells by western blot. Curcumin treatment upregulated miR-206 expression levels in the peripheral blood of patients with prolactinoma and in GH3 cells. Knockdown of miR-206 expression enhanced the proliferation and invasive ability of GH3 cells, while curcumin treatment effectively inhibited the aberrant biological behavior of GH3 cells enhanced by miR-206 knockdown. miR-206 knockdown also activated the Akt/mTOR signaling pathway and inhibited autophagy in GH3 cells, and these changes were effectively reversed by curcumin treatment. Thus, curcumin inhibited the Akt/mTOR signaling pathway and promoted cell autophagy by miR-206 upregulation, resulting in antitumor effects that inhibited prolactinoma cell proliferation and invasion.
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