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Background: Non‐small cell lung cancer (NSCLC) is a leading subtype in lung cancer, with high morbidities and mortalities worldwide. microRNA (miRNA) has appeared to play indispensable roles in a variety of solid carcinomas. The current study focused on the functions of miR‐100 in NSCLC. Methods: qRT‐PCR was performed to detect miR‐100 and HOXA1 expressions in NSCLC tissues and cells. MTT and transwell assays were used to determine the functions of miR‐100 in NSCLC cell proliferation, invasion and migration abilities. Western blot was used to measure related protein expressions. Results: qRT‐PCR results showed that miR‐100 expressions were dramatically decreased in NSCLC tissues. MTT assays indicated that miR‐100 restoration inhibited NSCLC cell proliferation. Furthermore, transwell assay was performed to determine the impacts of miR‐100 on NSCLC invasion and migration abilities. As expected, the invasion and migration capacities were significantly repressed. Direct interactions between HOXA1 and miR‐100 were also verified via dual‐luciferase reporter assays. Western blot analysis demonstrated that miR‐100 exerted suppressive functions via regulating EMT and Wnt/β‐catenin in NSCLC cells. Conclusions: Our results showed that miR‐100 served antitumor roles in NSCLC, providing new evidence of miR‐100 as a promising therapeutic biomarker in NSCLC. [ABSTRACT FROM AUTHOR]

Background: Non‐small cell lung cancer (NSCLC) accounts for 85% of lung cancer which is the most frequently diagnosed malignancy in China. Colon cancer associated transcript 1 (CCAT1) acts as an oncogene in enhancing tumor progression. However, the effects of CCAT1 in NSCLC remain unclear. The purpose of this study was to explore the role of CCAT1 in NSCLC. Methods: Wound healing and transwell assays were performed to measure cell migration. RT‐qPCR was employed to calculate the mRNA level of CCAT1 and miR‐490. Results: High expression of CCAT1 was observed in NSCLC tissues and cells, with low expression of miR‐490. CCAT1 promoted the proliferation and metastasis of H1299 and A549 cells, while miR‐490 had the opposite effect. CCAT1 could specifically bind to miR‐490 and regulate its expression. MiR‐490 partially reversed the inhibitory effect of CCAT1 on cell proliferation and metastasis. Conclusions: The CCAT1/miR‐490 molecular axis has been shown to be important for the treatment of NSCLC. [ABSTRACT FROM AUTHOR]