OBJECTIVE: Different effects of microRNA-495 (miR-495) on human cancers have been exhibited in recent years. However, the specific function of miR-495 remains uncertain in non-small-cell lung cancer (NSCLC). Thus, we aim to explore the role of miR-495 in NSCLC. PATIENTS AND METHODS: The expressions of miR-495 and transcription factor 4 (TCF4) were detected through quantitative Real-time polymerase chain reaction (qRT-PCR) assay. Western blot was used to measure the protein expression of relative genes. The relationship between miR-495 and TCF4 was testified by the dual-luciferase reporter gene assay. The function of miR-495 was investigated through cell counting kit-8 (CCK-8) assay and transwell assay. RESULTS: MiR-495 was downregulated in NSCLC tissues. Overexpression of miR-495 inhibited the migration, invasion and proliferation of NSCLC cells. Further, TCF4 was a direct target gene of miR-495. TCF4 was highly expressed in NSCLC tissues. In addition, miR-495 inhibited the progression of NSCLC through targeting TCF4. Furthermore, miR-495 inhibited EMT and Wnt/β-catenin pathway in NSCLC. CONCLUSIONS: MiR-495 inhibited the progression of NSCLC by targeting TCF4 and inactivating Wnt/β-catenin pathway.
OBJECTIVE: Different effects of microRNA-495 (miR-495) on humancancers have been exhibited in recent years. However, the specific function of miR-495 remains uncertain in non-small-cell lung cancer (NSCLC). Thus, we aim to explore the role of miR-495 in NSCLC. PATIENTS AND METHODS: The expressions of miR-495 and transcription factor 4 (TCF4) were detected through quantitative Real-time polymerase chain reaction (qRT-PCR) assay. Western blot was used to measure the protein expression of relative genes. The relationship between miR-495 and TCF4 was testified by the dual-luciferase reporter gene assay. The function of miR-495 was investigated through cell counting kit-8 (CCK-8) assay and transwell assay. RESULTS:MiR-495 was downregulated in NSCLC tissues. Overexpression of miR-495 inhibited the migration, invasion and proliferation of NSCLC cells. Further, TCF4 was a direct target gene of miR-495. TCF4 was highly expressed in NSCLC tissues. In addition, miR-495 inhibited the progression of NSCLC through targeting TCF4. Furthermore, miR-495 inhibited EMT and Wnt/β-catenin pathway in NSCLC. CONCLUSIONS:MiR-495 inhibited the progression of NSCLC by targeting TCF4 and inactivating Wnt/β-catenin pathway.