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Silencing circPVT1 enhances radiosensitivity in non-small cell lung cancer by sponging microRNA-1208.

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机构: [1]Department of Oncology, The First People’s Hospital of Qujing/The Qujing Affiliated Hospital of Kunming Medical University, Qujing, Yunnan, China [2]Department of Thoracic Surgery, The First People’s Hospital of Qujing/The Qujing Affiliated Hospital of Kunming Medical University, Qujing, Yunnan, China [3]Department of Radiation Oncology, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, China [4]Institute of Respiratory Medicine, Chinese Academy of Medicine Sciences, Beijing, China [5]National Center for Respiratory Disease, Beijing, China
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关键词: NSCLC circPVT1 miR-1208 radiosensitivity PI3K/AKT/mTOR signaling

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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 towards 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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出版当年[2021]版:
大类 | 3 区 医学
小类 | 3 区 肿瘤学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 肿瘤学
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出版当年[2020]版:
Q2 ONCOLOGY
最新[2023]版:
Q3 ONCOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2020版] 出版当年五年平均 出版前一年[2019版] 出版后一年[2021版]

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第一作者机构: [1]Department of Oncology, The First People’s Hospital of Qujing/The Qujing Affiliated Hospital of Kunming Medical University, Qujing, Yunnan, China
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通讯机构: [2]Department of Thoracic Surgery, The First People’s Hospital of Qujing/The Qujing Affiliated Hospital of Kunming Medical University, Qujing, Yunnan, China [3]Department of Radiation Oncology, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, China [4]Institute of Respiratory Medicine, Chinese Academy of Medicine Sciences, Beijing, China [5]National Center for Respiratory Disease, Beijing, China [*1]Department of Thoracic Surgery, The First People’s Hospital of Qujing/The Qujing Affiliated Hospital of Kunming Medical University, No.1 Yuanlin Road, Qilin District, Qujing 655000, Yunnan, China. [*2]Department of Radiation Oncology, Center of Respiratory Medicine, China-Japan Friendship Hospital.Institute of Respiratory Medicine, Chinese Academy of Medicine Sciences.National Center for Respiratory Disease, No.2 Yinghuadong Street, Chaoyang, Beijing 100029, China.
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