SP1 induced long non-coding RNA LINC00958 overexpression facilitate cell proliferation, migration and invasion in lung adenocarcinoma via mediating miR-625-5p/CPSF7 axis

Longhai Yang; Lili Li; Zizi Zhou; Yi Liu; Jinyuan Sun; Xiaoming Zhang; Huiyu Pan; Song Liu

doi:10.1186/s12935-020-1099-0

SP1 induced long non-coding RNA LINC00958 overexpression facilitate cell proliferation, migration and invasion in lung adenocarcinoma via mediating miR-625-5p/CPSF7 axis

Cancer Cell Int. 2020 Jan 23:20:24. doi: 10.1186/s12935-020-1099-0. eCollection 2020.

Authors

Longhai Yang¹, Lili Li², Zizi Zhou¹, Yi Liu¹, Jinyuan Sun³, Xiaoming Zhang¹, Huiyu Pan¹, Song Liu³

Affiliations

¹ 1Department of Cardiothoracic Surgery, Shenzhen University General Hospital/Shenzhen University Clinical Medical Academy, No. 1098 Xueyuan Road, Xili University Town, Shenzhen, 518055 Guangdong China.
² 2Respiratory Medicine, Liaocheng People's Hospital of Shandong Province, Liaocheng, 252000 Shandong China.
³ 3Department of Respiratory Medicine, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, No. 1665 Kongjiang Road, Yangpu District, Shanghai, 200092 China.

Abstract

Background: Increasing evidences have underlined the importance of long non-coding RNAs (lncRNAs) in human malignancies. LINC00958 has been found involved in some cancers. However, the underlying mechanical performance of LINC00958 in lung adenocarcinoma (LAD) has not been explored yet.

Methods: The expression of relevant mRNA and protein were measured by qRT-PCR and western blot assays. EdU, colony formation, TUNEL and transwell assays were performed to investigate the function of LINC00958 on LAD progression. Luciferase reporter, RNA pull down and RIP assays were conducted to investigate the molecular mechanism of relevant RNAs.

Results: LINC00958 was found notably overexpressed in LAD, which was associated with the stimulation of its promoter activity induced by SP1. LINC00958 depletion dramatically inhibited LAD cell proliferation, migration and invasion capacities by acting as a miR-625-5p sponge. MiR-625-5p curbed LAD progression via targeting CPSF7 and down-regulating its expression. Mechanically, LINC00958 was identified as a competing endogenous RNA (ceRNA) and positively regulated the expression of CPSF7 via sponging miR-625-5p.

Conclusions: LINC00958 might drive LAD progression via mediating miR-625-5p/CPSF7 axis, indicating the potential of targeting LINC00958 for the treatment of LAD.

Keywords: CPSF7; LAD; LINC00958; SP1; miR-625-5p.