LncRNA-POIR knockdown promotes hepatocellular carcinoma sensitivity to sorafenib through upregulating miR-182-5p and inhibiting autophagy
作者机构：Jintan Affiliated Hospital of Jiangsu UniversityChangzhou213200China Tongde Hospital of Zhejiang ProvinceHangzhou310012China
出 版 物：《BIOCELL》 (生物细胞（英文）)
年 卷 期：2022年第46卷第6期
页 面：1493-1503页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：The study was supported by Zhejiang Provincial Nature Science Foundation of China(LR20H160001) Key R&D projects of Zhejiang Province(2020C03G5263593) Zhejiang Provincial Ten Thousand Plan for Young Top Talents(2018) Training objects of health innovative talents of Zhejiang Health(2018) Key Project Co-constructed by Zhejiang Province and Ministry(WKJ-ZJ-1916),Natural Science Foundation of China(81972693,81802383,81972674,81673809 and 31900543) Zhejiang Provincial Traditional Chinese Medicine Science and Technology Project(2020ZZ004)
主 题：Hepatocellular carcinoma lncRNA-POIR miR-182-5p Resistance Autophagy
摘 要：Although sorafenib has been found to prolong the survival time of patients with hepatocellular carcinoma(HCC),sorafenib resistance remains an important *** studies have demonstrated that long noncoding RNAs(lncRNAs)contribute to drug resistance in a wide number of *** periodontal ligament stem cell(PDLSC)osteogenesis impairment-related lncRNA(POIR)is a recently defined lncRNA for which little is known regarding its *** study aimed to reveal the role of POIR in the development of HCC cell sorafenib *** level of POIR expression in patients and tumor cells was examined by Reverse transcription-quantitative polymerase chain reaction(RT-qPCR)***-8,EdU,and flow cytometry assay were adopted to examine cell viability,proliferation,and apoptosis,*** autophagy-associated protein expressions were determined by western blotting and autophagic flux *** results of this study exhibited increased POIR in HCC tissues and cells and may be correlated with sorafenib *** of POIR elevated sorafenib sensitivity by suppressing autophagy in HCC ***,POIR knockdown upregulated miR-182-5p,implying that miR-182-5p mediates POIR ***-182-5p overexpression significantly enhanced chemosensitivity to sorafenib,whereas miR-182-5p inhibition had the opposite *** sensitization of POIR siRNA to sorafenib was abolished by co-transfection with miR-182-5p *** findings provide a potential target for further clinical treatment of sorafenib-resistant HCC patients.
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