miR-101-3p sensitizes non-small cell lung cancer cells to irradiation

Open Medicine

Wang Ying¹  Qin Meilin²  Qu Zhenjie²  Li Zhonghui²  Zhang Hua² 

[1] Department of Gerontology, the Third Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, China;Department of Oncology, the Third Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, China;

关键词: mir-101-3p;    mtor;    nsclc;    irradiation;   

DOI  :  10.1515/med-2020-0044

来源: DOAJ

【 摘 要 】

Recent studies have revealed that microRNAs regulate radiosensitivity of non-small cell lung cancer (NSCLC). The aim of this study was to investigate whether miR-101-3p is correlated with radiosensitivity of NSCLC. According to our results, miR-101-3p was downregulated in NSCLC tissues and cell lines. Moreover, miR-101-3p was decreased in A549 cells’ response to irradiation in a dose-dependent manner. Upregulation of miR-101-3p decreased survival fraction and colony formation rate and increased irradiation-induced apoptosis in irradiation-resistant cells, while miR-101-3p depletion had the opposite effects in irradiation-sensitive cells. Furthermore, mechanistic target of rapamycin (mTOR) is a target gene of miR-101-3p. The expressions of mTOR, p-mTOR, and p-S6 were curbed by overexpression of miR-101-3p in A549R cells, which was enhanced by repression of miR-101-3p in A549 cells. Intriguingly, elevation in mTOR abated miR-101-3p upregulation-induced increase in irradiation sensitivity in irradiation-resistant cell line. In contrast, rapamycin undermined miR-101-3p inhibitor-mediated reduction of irradiation sensitivity in irradiation-sensitive cell line. Besides, miR-101-3p overexpression enhanced the efficacy of radiation in an NSCLC xenograft mouse model. In conclusion, miR-101-3p sensitized A549 cells to irradiation via inhibition of mTOR-signaling pathway.

【 授权许可】

Unknown