LINC00632 inhibits the malignant development of non-small cell lung cancer by downregulating miR-1203.

PURPOSE:To uncover the role of LINC00632 in influencing metastasis of non-small cell lung cancer (NSCLC) and the potential molecular mechanism. METHODS:LINC00632 levels in paired NSCLC and paracancer tissues were detected. The correlation between LINC00632 level and pathological features of NSCLC was analyzed. In vitro proliferative and migratory abilities in NSCLC regulated by LINC00632 were assessed. In addition, nude mice bearing NSCLC were prepared to explore the in vivo effect of LINC00632 on tumor growth. The targeting relationship between LINC00632 and miR-1203 was confirmed by dual-luciferase reporter assay. The involvement of miR-1203 in regulating NSCLC cell phenotypes was finally explored. RESULTS:LINC00632 was lowly expressed in NSCLC tissues. Low level of LINC00632 indicated high rates of lymph node metastasis and distant metastasis, as well as poor prognosis in NSCLC. Overexpression of LINC00632 suppressed in vitro proliferative and migratory abilities in NSCLC. Moreover, overexpression of LINC00632 inhibited tumor growth in nude mice bearing NSCLC. MiR-1203 was the downstream target of LINC00632, which was upregulated in NSCLC tissues. The inhibitory effects of LINC00632 on cell growth and metastasis in NSCLC were abolished by overexpression of miR-1203 levels. CONCLUSIONS:LINC00632 is downregulated in NSCLC samples, which is closely linked to metastasis and prognosis in NSCLC patients. It inhibits the malignant development of NSCLC by negatively regulating miR-1203 level.

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