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Background:  Lung cancer is the most common malignant tumor worldwide. Accumulating results have shown that long non-coding RNAs (lncRNAs) play a key role in tumorigenesis.   Patients and Methods:  A total of 163 tumor tissues were collected from non-small cell lung cancer (NSCLC) patients from West China Hospital of Sichuan University.  LincRNA00494  is a novel lncRNA, and its expression and biological effect in NSCLC were reported in this study. NSCLC cell lines were used in this study.   Results:   LincRNA00494  is mainly distributed in the cytoplasm.  LincRNA00494  was downregulated in the tumor tissues compared with the adjacent non-tumor tissues.  LincRNA00494  expression was positively correlated with SRCIN1 expression ( R  = 0.57,  P  < 0.05). Silencing of  LincRNA00494  in the cell lines substantially decreased SRCIN1 expression at the mRNA and protein levels, whereas overexpression of  LincRNA00494  enhanced the SRCIN1 levels. miR-150-3p significantly decreased the luciferase signals of  LincRNA00494  and SRCIN1 reporters. After transfection with miR-150-3p mimics and miR-150-3p inhibitor, overexpression of  LincRNA00494  decreased the proliferation of the H358 (36%) and H1299 (29%) cell lines compared with that of the control cells, as shown by CCK-8 assays, whereas silencing  LincRNA00494  promoted the proliferation of the H358 (47%) and H1299 (35%) cells. Tumor growth from LincRNA00494-overexpressing xenografts was significantly decreased; additionally, LincRNA00494 silencing substantially increased tumor growth compared with that of the control cells.   Conclusions:  Functional experiments revealed that  LincRNA00494  inhibited NSCLC cell proliferation, which might be related to the suppression of SRCIN1, a tumor suppressor gene, by acting as a decoy for miR-150-3p. The data showed that  LincRNA00494  might have antineoplastic effects during NSCLC tumorigenesis through its role as a ceRNA.

LincRNA00494 Suppresses Non-small Cell Lung Cancer Cell Proliferation by Regulating SRCIN1 Expression as a ceRNA