详细信息
miR-101-3p sensitizes hepatocellular carcinoma cells to oxaliplatin by inhibiting Beclin-1-mediated autophagy ( SCI-EXPANDED收录) 被引量:15
文献类型:期刊文献
英文题名:miR-101-3p sensitizes hepatocellular carcinoma cells to oxaliplatin by inhibiting Beclin-1-mediated autophagy
作者:Sun, Wenping[1];Zhang, Qiang[2];Wu, Zhiwei[3];Xue, Na[3]
第一作者:Sun, Wenping
通信作者:Wu, ZW[1]
机构:[1]Gansu Prov Canc Hosp, Dept Abdominal Surg, Lanzhou, Gansu, Peoples R China;[2]Gansu Prov Canc Hosp, Dept Urol, Lanzhou, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Coll Basic Med, 35 East Dingxi Rd, Lanzhou, Gansu, Peoples R China
第一机构:Gansu Prov Canc Hosp, Dept Abdominal Surg, Lanzhou, Gansu, Peoples R China
通信机构:[1]corresponding author), Gansu Univ Chinese Med, Coll Basic Med, 35 East Dingxi Rd, Lanzhou, Gansu, Peoples R China.|[107351d2d02a88e1f325f]甘肃中医药大学基础医学院(敦煌医学研究所);[10735]甘肃中医药大学;
年份:2019
卷号:12
期号:6
起止页码:2056
外文期刊名:INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
收录:;WOS:【SCI-EXPANDED(收录号:WOS:000473287100012)】;
基金:This research was funded by the Natural Science Foundation of Gansu Province (no. 18JR-3RA200), the Gansu Provincial Administration of Traditional Chinese Medicine (no. GZK-2017-5), the Provincial-Level Key Laboratory for Molecular Medicine of Major Diseases, and the Prevention and Treatment with Traditional Chinese Medicine Research in Gansu Colleges and Universities (no. FZYX15-16-1).
语种:英文
外文关键词:miR-101-3p; Beclin-1; autophagy; oxaliplatin; hepatocellular carcinoma
摘要:Background: Increasing evidence has shown that autophagy can contribute to drug resistance. Whether microRNA-101-3p (miR-101-3p) participates in oxaliplatin (OXA) resistance via modulating Beclin-1-mediated autophagy in hepatocellular carcinoma (HCC) has not been reported. Methods: OXA-resistant Huh7 cells (Huh7/OXA) or HepG2 cells (HepG2/OXA) and OXA-sensitive Huh7 or HepG2 cells were treated with OXA in various concentrations. The expressions of miR-101-3p and Beclin-1 were monitored using qRT-PCR. Western blot was used to evaluate cell autophagy. Cell viability and the IC50 of OXA were determined using an MTT assay. Cell apoptosis was evaluated by flow cytometry. A luciferase reporter assay was introduced to confirm the relationship between miR-101-3p and Beclin-1. Results: miR-101-3p was decreased in HCC resistant tissues and cells. Moreover, an increased expression of miR-101-3p reduced cell viability and the IC50 of OXA, and it promoted cell apoptosis in Huh7/OXA and HepG2/OXA cells. miR-101-3p negatively modulated the expression of Beclin-1. Interestingly, the overexpression of Beclin-1 receded the effect of the ectopic expression of miR-101-3p in OXA-resistant HCC cells. In OXA-sensitive Huh7 and HepG2 cells, OXA significantly increased the expressions of LC3 and Beclin-1, and it decreased the abundance of p62. Furthermore, OXA markedly blocked cell viability, which was exacerbated by the introduction of the autophagy inhibitor CQ. Additionally, the elevated expression of miR-101-3p suppressed cell autophagy by inhibiting the expression of LC3 and Beclin-1 and facilitating the expression of p62. Conclusion: miR-101-3p is responsible for the sensitivity of HCC cells to OXA by inhibiting Beclin-l-mediated autophagy.
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