LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1
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RESEARCH
Open Access
LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 Qiming Shen, Yanbin Sun and Shun Xu*
Abstract Background: Non-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. Methods: Thirty NSCLC patients were recruited between April 2012 and April 2016. Luciferase reporter assay, qRTPCR, Cell Counting Kit-8 (CCK-8), Transwell migration assay, RNA pull-down assay, western blotting, 5-ethynyl-29deoxyuridine (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. Results: We 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. Conclusion: These results provide a comprehensive analysis of the roles of LINC01503 as a competing endogenous RNA (ceRNA) in NSCLC progression. Keywords: LINC01503, miR-342-3p, Non-small-cell lung cancer, LASP1
Background Non-small cell lung cancer (NSCLC) is one of the major types of lung cancer, which is a quite prevalent human disease all over the world [1]. Extensive efforts have been made to discover new therapeutic targets for the treatment of NSCLC [2, 3]. However, as the early symptoms of NSCLC are not obvious, a large portion of NSCLC patients was diagnosed at late stages, with high malignancy and low treatment opportunities [1, 4]. The current overall 5-year survival rate of NSCLC patients * Correspondence: [email protected] Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Road, Heping Area, Shenyang 110001, China
still remains unsatisfactory [5]. In this study, we focused to understand the pathogenesis of NSCLC, as well as to investigate new therapeutic targets based on the tumorigenesis of NSCLC. Long noncoding RNAs (lncRNAs, > 200 nt) are a major subtype of non-coding RNAs that cannot translate to proteins [6, 7]. A large number of lncRNAs have been discovered to play vital roles in tumorigenesis, with an unignorable impact in many biological procedures such as cell proliferation, cell cycle, cell death, as well as tumor metastasis [8, 9]. Previous studies have revealed the expression profiles of several lncRNAs that participate closely in the tumorigenesis of NSCLC, including
© The Author(s). 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which
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