Overexpression of miR-758 inhibited proliferation, migration, invasion, and promoted apoptosis of non-small cell lung cancer cells by negatively regulating HMGB

被引:24
作者
Zhou, Guo-Hua [1 ]
Lu, Yi-Yu [2 ]
Xie, Jing-Lian [1 ]
Gao, Zi-Kun [1 ]
Wu, Xiao-Bo [1 ]
Yao, Wei-Shen [1 ]
Gu, Wei-Guang [2 ]
机构
[1] Southern Med Univ, Nanhai Hosp, Dept Thorac Surg, Peoples Hosp Nanhai Dist, Foshan 528244, Peoples R China
[2] Southern Med Univ, Dept Oncol, Nanhai Hosp, Peoples Hosp Nanhai Dist, Foshan 528244, Peoples R China
关键词
PROGNOSTIC MARKER; DRUG-SENSITIVITY; POOR-PROGNOSIS; UP-REGULATION; EXPRESSION; NSCLC; GROWTH; SUPPRESSES; CHEMOTHERAPY; LEUKEMIA;
D O I
10.1042/BSR20180855
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Non-small cell lung cancer (NSCLC) is one of the most fatal types of cancer with significant mortality and morbidity worldwide. MicroRNAs (miRs) have been confirmed to have positive functions in NSCLC. In the present study, we try to explore the role of miR-758 in proliferation, migration, invasion, and apoptosis of NSCLC cells by regulating high-mobility group box (HMGB) 3 (HMGB3.) NSCLC and adjacent tissues were collected. Reverse transcription quantitative PCR (RT-qPCR) was employed to detect expression of miR-758 and HMGB3 in NSCLC and adjacent tissues, in BEAS-2B cells and NSCLC cell lines. The targetted relationship between miR-758 and HMGB3 was identified by dual luciferase reporter gene assay. The effects of miR-758 on proliferation, migration, invasion, cell cycle, and apoptosis of A549 cells. MiR-758 expression was lower in NSCLC tissues, which was opposite to HMGB3 expression. The results also demonstrated that miR-758 can target HMGB3. The cells transfected with miR-758 mimic had decreased HMGB3 expression, proliferation, migration, and invasion, with more arrested cells in G1 phase and increased apoptosis. Our results supported that the overexpression of miR-758 inhibits proliferation, migration, and invasion, and promotes apoptosis of NSCLC cells by negative regulating HMGB2. The present study may provide a novel target for NSCLC treatment.
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页数:13
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