Pinocembrin inhibits migration and invasion of non-small cell lung cancer cells by inhibiting STAT3 signaling

Abstract

Abstract Background STAT3 activation plays a pivotal role in promoting ETM-mediated tumor progression and metastasis and has been considered as a target for the treatment of cancer. Pinocembrin, a natural dihydroxyflavanone found in propolis and honey, has antioxidant and vasodilating properties. In this study, we aim to investigate the role of pinocembrin in inhibiting cells migration and invasion via regulating STAT3 signaling in non-small cell lung cancer cells. Methods A549 cells migration and invasion were determined by hematoxylin staining. Relative expression of ETM-related proteins and invasive proteins in A549 cells were determined by western blot. STAT3 activity was evaluated by luciferase assay. Overexpression of STAT3 were used to assess the role of pinocembrin in regulating STAT3. Results The number of migrating and invasive cells were significantly reduced by the treatment of pinocembrin. The protein level of E-cadherin was upregulated, and the protein levels of N-cadherin and vimentin were downregulated by pinocembrin. The phosphorylation and activation of STAT3 were blocked by pinocembrin. Overexpression of STAT3 reversed the inhibitory effects of pinocembrin on cells migration and invasion. Conclusion Our results suggested that pinocembrin can inhibit STAT3 activation mediated ETM transformation, thereby attenuating migration and invasion in non-small lung cancer cells. Given the significance of STAT3 activation, our findings showed that pinocembrin, by inhibiting STAT3 activation mechanistically, could potentially serve as an effective therapeutic approach for the treatment and management of lung cancer in clinical.