期刊
CELL CYCLE
卷 19, 期 3, 页码 300-316出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2019.1708016
关键词
Non-small cell lung cancer; LncRNA SBF2-AS1; MicroRNA-302a; Muscleblind-like 3; Proliferation; Apoptosis; Radiosensitivity
类别
资金
- General Program of Natural Science Foundation of Liaoning Province [2015020464]
- Major Science and Technology Platform of Liaoning Higher Institution [2916009]
- Science Research Foundation for Absorbed Talents Program of Liaoning Cancer Hospital
- Special Project of Applied Technology of Population and Health by Shenyang Science and Technology Plan [18-014-4-04]
Background: Long non-coding RNAs (lncRNAs) have been reported to participate in many diseases including non-small cell lung cancer (NSCLC), thus our objective was to investigate the impact of lncRNA SBF2-AS1 modulating microRNA-302a (miR-302a) expression on radiosensitivity of NSCLC. Methods: The expression of SBF2-AS1, miR-302a and muscleblind-like 3 (MBNL3) in NSCLC tissues of the radiotherapy-sensitive and radiotherapy-resistant groups was tested. The radiosensitivity of parent and resistant strains (NCI-H1299 and NCI-H1299(R) cells) was detected. Further, cells were treated with si-SBF2-AS1 and miR-302a mimics to determine their roles in proliferation and apoptosis of parent strain and resistant strain cells as well as transfected cells. The in-vivo growth capacity of the cells and the effect of radiotherapy on tumor size of NSCLC were detected. Results: Up-regulated SBF2-AS1 and MBNL3 and down-regulated miR-302a in NSCLC tissues of the radiotherapy resistant group. Overexpression of SBF2-AS1 and MBNL3 and low expression of miR-302a were witnessed in NCI-H1299(R) cells. Down-regulated SBF2-AS1 or up-regulated miR-302a suppressed the proliferation while boosted the apoptosis of NCI-H1299 cells and decreased the radioresistance of the NCI-H1299(R) cells. Silencing SBF2-AS1 or up-regulating miR-302a restrained tumor growth in vivo. Conclusion: Our study presents that high expression of miR-302a or inhibition of SBF2-AS1 can enhance the radiosensitivity and apoptosis of NSCLC cells through downregulation of MBNL3, which is a therapeutic target for NSCLC.
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