Long non-coding RNA FOXO1 inhibits lung cancer cell growth through down-regulating PI3K/AKT signaling pathway
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 22، شماره: 5
سال انتشار: 1398
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 281
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شناسه ملی سند علمی:
JR_IJBMS-22-5_005
تاریخ نمایه سازی: 20 مهر 1398
چکیده مقاله:
Objective(s): Lung cancer is one of the most common malignant tumors, which seriously threatens the health and life of the people. Recently, a novel long non-coding RNA (lncRNA) termed lncFOXO1 was found and investigated in breast cancer. However, the effect of lncFOXO1 on lung cancer is still ambiguous. The current study aimed to uncover the functions of lncFOXO1 in lung cancer cell proliferation, metastasis and apoptosis.Materials and Methods: LncFOXO1 expression levels in lung cancer tissues or cells were detected using qRT-PCR. Then, overexpression and knockdown vectors of lncFOXO1 were transfected into A549 cells to investigate the effect of lncFOXO1 on cell proliferation, invasion, migration and apoptosis. These experiments were assessed using MTT, colony formation, transwell, flow cytometry and western blot assays, respectively. In vivo experiment was performed to examine the tumor weight using Xenograft tumor model assay. The important pathway of PI3K/AKT was finally examined using western blot. Results: The decreased expression level of lncFOXO1 was observed in lung cancer tissues and cells (A549, H460, HCC827 and H1299). Knockdown of lncFOXO1 significantly promoted A549 cells viability, colony formation and invasion. However, lncFOXO1 overexpression obviously reversed the results. Moreover, lncFOXO1 overexpression induced A549 cells apoptosis by regulating Bax, cleaved-caspase-3 and Bcl-2. In vivo experiment revealed that lncFOXO1 overexpression inhibited tumor weight. Furthermore, lncFOXO1 knockdown promoted colony formation and mediated Myc and Cyclin D1 expressions by regulating PI3K/AKT signaling pathway.Conclusion: LncFOXO1 inhibited lung cancer cell proliferation, metastasis, and induced apoptosis through down-regulating PI3K/AKT pathway.
کلیدواژه ها:
نویسندگان
Xiaoqian Ding
Department of Respiratory, The Affiliated Hospital of Qingdao University, Qingdao ۲۶۶۰۰۰, Shandong, China
Qiang Wang
Department of Respiratory, The Affiliated Hospital of Qingdao University, Qingdao ۲۶۶۰۰۰, Shandong, China
Li Tong
Department of Respiratory, The Affiliated Hospital of Qingdao University, Qingdao ۲۶۶۰۰۰, Shandong, China
Xin Si
Department of Radiology, Qingdao West Coast New Area Central Hospital, Qingdao ۲۶۶۵۵۵, Shandong, China
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