Document Type : Original Article
Department of Operation, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, China
Department of Thoracic Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, China
Department of Interventional Radiology, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, China
Objective: Dysregulation of long non-coding RNAs (lncRNAs) is associated with the progression of non-small cell lung cancer (NSCLC). This study aimed to investigate the role of long intergenic non-protein coding RNA 174 (LINC00174)
Materials and Methods: In this experimental study, LINC00174 expression in NSCLC tissues and cell lines was investigated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Besides, cell counting kit-8 (CCK8), 5-bromo-2'-deoxyuridine (BrdU). Transwell and Flow Cytometry assays were applied to detect the regulatory function of LINC00174 on the growth, migration and apoptosis of NSCLC cells. Bioinformatics analysis, dual luciferase
reporter gene assay and RNA immunoprecipitation (RIP) assay predicted and verified the targeting relationship between
LINC00174 and miR-31-5p, and between miR-31-5p and the 3´-untranslated region (3´UTR) of large tumor suppressor kinase 2 (LATS2), respectively. Western blotting was performed to detect the regulatory function of LINC00174 and miR-31-5p on LATS2 protein expression.
Results: Compared with that in normal lung tissues, LINC00174 expression in NSCLC tissues and cell lines was reduced. LINC00174 expression was negatively associated with the TNM stage of the patients. Functional experiments showed that LINC00174 overexpression inhibited NSCLC cell multiplication and migration, and induced apoptosis. Furthermore, LINC00174 targeted miR-31-5p and repressed its expression. Additionally, LINC00174 upregulated LATS2 expression through competitively binding to miR-31-5p.
Conclusion: LINC00174, as a competitive endogenous RNA, elevates LATS2 expression by adsorbing miR-31-5p,
thereby inhibiting the viability and migration of NSCLC cells, and promoting apoptosis.