Pinocembrin inhibits migration and invasion of nonsmall cell lung cancer cells by inhibiting STAT3 signaling
Abstract
Background: In cancer treatment, targeting the activation of signal transducer and activator of transcription 3 (STAT3) is crucial as it promotes tumor progression and metastasis through the process of epithelial-mesenchymal transition (EMT). Pinocembrin, a dihydroxyflavanone found naturally in propolis and honey, is known for its antioxidant and vasodilating properties. The objective of this study is to explore the potential of pinocembrin in regulating the STAT3 signaling pathway to inhibit migration and invasion of nonsmall cell lung cancer (NSCLC) cells.
Methods: Hematoxylin staining was used to determine the migration and invasion of A549 cells. The relative expression of EMT-related proteins and invasive proteins in A549 cells was determined by Western blot analysis. STAT3 activity was evaluated using a luciferase assay. Overexpression of STAT3 was utilized to assess the role of pinocembrin in regulating STAT3.
Results: Pinocembrin treatment (50 μM) significantly reduced the number of migrating and invasive cells. Pinocembrin upregulated the protein level of E-cadherin and downregulated the protein levels of N-cadherin and vimentin. Additionally, pinocembrin blocked the phosphorylation and activation of STAT3. Overexpression of STAT3 reversed the inhibitory effects of pinocembrin on cell migration and invasion.
Conclusion: Our study demonstrates that pinocembrin can inhibit the activation of STAT3, which is associated with EMT and thereby attenuate migration and invasion in NSCLC cells.
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