LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1

Respiratory Research

Yanbin Sun¹  Shun Xu¹  Qiming Shen¹ 

[1] Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Road, Heping Area, 110001, Shenyang, China;

关键词: LINC01503;    miR-342-3p;    Non-small-cell lung cancer;    LASP1;   

DOI  :  10.1186/s12931-020-01464-3

来源: Springer

【 摘 要 】

BackgroundNon-small cell lung cancer (NSCLC) is one of the major types of lung cancer, which is a prevalent human disease all over the world. LncRNA LINC01503 is a super-enhancer-driven long non-coding RNA that is dysregulated in several types of human cancer. However, its role in NSCLC remains unknown.MethodsThirty NSCLC patients were recruited between April 2012 and April 2016. Luciferase reporter assay, qRT-PCR, Cell Counting Kit-8 (CCK-8), Transwell migration assay, RNA pull-down assay, western blotting, 5-ethynyl-29-deoxyuridine (EdU) assays, and flow cytometry were utilized to characterize the roles and relationships among LINC01503, miR-342-3p, and LASP1 in NSCLC. The transplanted mouse model was built to examine their biological functions in vivo.ResultsWe demonstrated that the expression of lncRNA LINC01503 and LIM and SH3 domain protein 1 (LASP1) were upregulated and miR-342-3p was downregulated in NSCLC samples and cell lines. Functional experiments revealed that inhibiting the expression of LINC01503 or over-expression of miR-342-3p inhibited NSCLC growth and metastasis both in vitro and in vivo. In addition, LINC01503 could bind to miR-342-3p and affect the expression of LASP1.ConclusionThese results provide a comprehensive analysis of the roles of LINC01503 as a competing endogenous RNA (ceRNA) in NSCLC progression.

【 授权许可】

CC BY