ESC reverses epithelial mesenchymal transition induced by transforming growth factor-β via inhibition of Smad signal pathway in HepG2 liver cancer cells.

Background: Epithelial mesenchymal transition (EMT) mediated by TGF-β pays an important role in malignant tumor acquired abilities of migration and invasion. Our previous study showed that the extract of Stellera chamaejasme L. (ESC) was against proliferation of a variety of tumor cells, but there were no studies in the effects of ESC on EMT in tumor cells. In this study, TGF-β was adopted to induce EMT in HepG2 cells and the influence of ESC on EMT was observed.

Methods: MTT assay was used to observe the cell viability. Wound healing assay and transwell assay were used to observe the migration and invasion activities. Western blot and immunofluorescence methods were used to observe the expression of proteins.

Results: We found that HepG2 cells induced by TGF-β showed mesenchymal morphology, down-regulation of epithelial marker E-cadherin and up-regulation of mesenchymal marker Vimentin, indicating that TGF-β could mediate epithelial mesenchymal induction in HepG2 cells. ESC could reverse the mesenchymal morphology and regulate expressions of marker proteins in HepG2 induced by TGF-β and significantly inhibit TGF-β induced HepG2 cell migration and invasion. We further found that ESC could also significantly depress Smad2 phosphorylation and nuclear translocation, and ESC had coordination with SB432542, a specific inhibitor of TβRI kinases.

Conclusions: These results suggested that the ESC could reverse epithelial mesenchymal transition induced by TGF-β via inhibition Smad2 signaling pathway.