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2015 ; 15
(ä): 114
Nephropedia Template TP
gab.com Text
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Twit Text #
English Wikipedia
ESC reverses epithelial mesenchymal transition induced by transforming growth
factor-? via inhibition of Smad signal pathway in HepG2 liver cancer cells
#MMPMID26692820
Liu XN
; Wang S
; Yang Q
; Wang YJ
; Chen DX
; Zhu XX
Cancer Cell Int
2015[]; 15
(ä): 114
PMID26692820
show ga
BACKGROUND: Epithelial mesenchymal transition (EMT) mediated by TGF-? 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-? 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-? showed
mesenchymal morphology, down-regulation of epithelial marker E-cadherin and
up-regulation of mesenchymal marker Vimentin, indicating that TGF-? 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-? and significantly inhibit TGF-? 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 T?RI kinases. CONCLUSIONS: These results
suggested that the ESC could reverse epithelial mesenchymal transition induced by
TGF-? via inhibition Smad2 signaling pathway.