Effect and mechanism of lncRNA UCA1 target regulating miR-185-5p on non-small cell lung cancerA549 cell / 中国肿瘤生物治疗杂志

ABSTRACT

@# Objective: To investigate the effect and underlying mechanism of Long non-coding RNAurothelial carcinoma associated 1 (lncRNA UCA1) on proliferation, invasion and migration of non-small cell lung cancer (NSCLC) A549 cells. Methods: NSCLS A549 cells were cultured and transfected with lentivirus; RT-PCR was employed to detect the levels of UCA1 in A549 cells. The relationship between UCA1 and miR-185-5p was validated by luciferase reporter assays. Cell viability ofA549 cells was measured by MTT. Cell invasion and migration were determined by Transwell and Wound healing assay, respectively; and western blotting was performed for measuring the levels of Wnt1/β-catenin pathway-related proteins. Results: sh-UCA1 significantly decreased UCA1 expression and increased miR-185-5p expression in A549 cells (all P<0.05). miR-185 inhibitor attenuated the promotion effect of sh-UCA1 on miR-1855p (P<0.05). UCA1 could significantly down-regulate miR-185-5p expression in A549 cells (P<0.05), which was reversed by miR-185 mimic (P<0.05). Luciferase reporter assay validated the binding site on UCA1 to link miR-185-5p. sh-UCA1 significantly inhibited cell proliferation, invasion and migration ofA549 cells (all P<0.05), and also decreased the protein levels of Wnt1, β-catenin and TCF-4 notably (all P<0.05); however, miR-185 inhibitor attenuated such inhibitory effects of sh-UCA1 (P<0.05). Conclusion: UCA1 could promote proliferation, invasion and migration of A549 cells through targeting miR-185-5p, and the mechanisms might be related with activation of Wnt1/β-catenin pathway.