Abstract
The aim of this study was to study the role of miR‐372‐3p in lung squamous cell carcinoma (LSCC) cell proliferation and invasion by suppressing FGF9. RT‐PCR was used to determine miR‐372‐3p and FGF9 mRNA expression in tissues and cells. Western blot was used to determine FGF9 expression in tissues and NCI‐H520 cell line. Dual luciferase reporter gene assay was conducted to confirm that FGF9 can be directly targeted by miR‐372‐3p. MTT, colony formation assays were conducted to investigate the effects of ectopic miR‐372‐3p and FGF9 expression on NCI‐H520 cell growth. Flow cytometry was used to analyze the influence of miR‐372‐3p and FGF9 expression on cell cycle distribution and apoptosis. Transwell assay was also conducted to see the effects of miR‐372‐3p and FGF9 expression on NCI‐H520 cell invasiveness. MiR‐372‐3p was found significantly overexpressed in both LSCC tissues and cell lines, whereas FGF9 mRNA was found underexpressed in LSCC tissues. MiR‐372‐3p directly bound to wild‐type FGF9 mRNA 3′UTR, therefore led to the reduction in FGF9 expression. The upregulation of FGF9 or the downregulation of miR‐372‐3p substantially retarded LSCC cell growth, mitosis, and invasion. MiR‐372‐3p enhanced LSCC cell proliferation and invasion through inhibiting FGF9.
Highlights
Lung cancer is the principal cause of deaths related to cancer worldwide [1]
Wang et al indicated that FGF9 was upregulated in patients with lung adenocarcinoma, and that aberrant FGF9 expression might inhibit the progression of lung adenocarcinoma [16]
FGF9 mRNA expression was determined by RT-PCR
Summary
Lung cancer is the principal cause of deaths related to cancer worldwide [1]. Non-small-cell lung cancers (NSCLC) account for 80% of lung cancer, and are classified into four subtypes according to their histological and pathological features: lung adenocarcinoma, lung squamous cell carcinoma (LSCC), lung large cell carcinoma, and lung neuroendocrine cancer [2, 3]. 40% of patients with NSCLC that are at advanced stage hardly survive more than 5 years despite of traditional chemotherapy, molecular-targeted therapy or chemoradiotherapy [2,3,4]. FGF9, belonging to the FGF family, its aberrant expression has been identified in diverse tumors, such as breast, prostate, endometrioid, and lung cancers, indicating its tumor biomarker role in various cancers [12,13,14,15]. Wang et al indicated that FGF9 was upregulated in patients with lung adenocarcinoma, and that aberrant FGF9 expression might inhibit the progression of lung adenocarcinoma [16]. Little is known about the role of FGF9 during LSCC
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