辐射敏感性
癌症研究
基因沉默
PI3K/AKT/mTOR通路
细胞生长
小RNA
抗辐射性
生物
细胞凋亡
细胞
化学
分子生物学
细胞培养
医学
放射治疗
内科学
基因
生物化学
遗传学
作者
Meifang Huang,Tianqian Li,Qing Wang,Chongxin Li,Huahua Zhou,Shengyi Deng,Zengbo Lv,Yongmei He,Bo Hou,Guangying Zhu
摘要
Radiotherapy is one of main useful therapies in non-small cell lung cancer (NSCLC). Nevertheless, the underlying mechanism between NSCLC cell radiosensitivity and effective treatment remains unclear.The aim is to explore the relationship between circular (circ) RNA and NSCLC cell radiosensitivity.CircRNA plasmacytoma variant translocation 1 (PVT1) and microRNA (miR)-1208 expression in NSCLC cells were assessed using quantitative reverse transcriptase PCR (qRT-PCR). NSCLC cells were transfected with si-PVT1 or miR-1208 inhibitor and then exposed to irradiation. Cellular biology behaviors were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL), colony formation, invasion and western blot. Additionally, binding between circPVT1 and miR-1208 was testified by dual-luciferase reporter and RIP assay.CircPVT1 was upregulated in NSCLC cells after irradiation treatment. Silencing circPVT1 induced inhibition of NSCLC cell growth and invasion, accompanied by cell apoptosis and γ-H2AX expression. Moreover, NSCLC cell proliferation and invasion was further inhibited by irradiation treatment in circPVT1-silenced cells, indicating a strong radiosensitivity of NSCLC cells. CircPVT1 functions as a competing endogenous RNA of miR-1208. Silencing miR-1208 reversed NSCLC cell sensitivity response to irradiation and activated PI3K/AKT/mTOR pathway in circPVT1-silenced cells.Silencing circPVT1 enhanced radiosensitivity of NSCLC cells by sponging miR-1208.
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