RESUMEN
OBJECTIVE: Curcumin has been reported to possess anti-tumor effects on multiple cancers, including lung cancer. However, the mechanisms of its anti-tumor effect on lung cancer have not been fully elucidated. Our study attempted to identify the effect of curcumin on A549 cells and further explore the potential mechanism. METHODS: Different concentrations of curcumin were exposed to A549 cells for 24 h and cell viability was measured by CCK-8 assay. The expression of UCA1 was overexpressed in A549 cells by transfection with pEX-UCA1. Cell proliferation was determined by BrdU staining and assessing the expression of CyclinD1 using western blot and RT-PCR assay. Apoptotic cells were measured by flow cytometry assay. Western blot was performed to assess the expression of apoptosis-related, Wnt and mTOR pathways-related factors. RESULTS: Curcumin incubation dramatically reduced viability of A549 cells in a dosage-dependent manner. Curcumin (0.6 µM) significantly reduced BrdU+-positive cells, declined the expression of CyclinD1, and enhanced cell apoptosis. Interestingly, we found that curcumin inhibited the expression of UCA1 and UCA1 overexpression abolished the effect of curcumin on cell apoptosis. In addition, we also found that curcumin inhibited Wnt and mTOR pathways through down-regulation of UCA1. CONCLUSION: We demonstrated that curcumin inhibited the growth of A549 cells through downregulation of UCA1, which might provide new insight for the treatment of lung cancer.