PLK1 promotes epithelial-mesenchymal transition of esophageal squamous cell carcinoma cells by stabilizing β-catenin
10.3969/j.issn.1001-1978.2014.12.026
- VernacularTitle:PLK1稳定β-catenin 促进食管鳞癌细胞上皮间质转化
- Author:
Jiyu JU
;
Wenjing YU
;
Zhiqin GAO
;
Weifen ZHANG
;
Changqing DU
;
Limei CHEN
;
Bo LIAN
;
Chunling ZHAO
- Publication Type:Journal Article
- Keywords:
PLK1;
esophageal squamous cell carcino-ma;
vimentin;
EMT;
β-catenin;
RNA interference
- From:
Chinese Pharmacological Bulletin
2014;(12):1748-1751
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of PLK1 on epithelial-mesenchymal transition (EMT)of human e-sophageal squamous cell carcinoma (ESCC)cells TE-1 5 and its relevant molecular mechanisms.Methods PLK1 overexpressed ESCC cells and control vector were used as the experimental cells.The expression of EMT-related protein markers E-cadherin and vimentin were measured by Western blot.vimentin mRNA was measured by Real-time PCR.Total cellular protein and nuclear protein were respectively extracted,and then they were used to detect the expression of β-catenin by Western blot.β-catenin siRNA and non-specific siR-NA were transiently transfected into the cell clones overexpressed PLK1 ,and then vimentin was detected by Western blot.β-catenin protein degradation com-plex was detected by immunoprecipitation and Western blot.Results The mesenchymal marker vimentin was distinctively upregulated and the epithelial marker E-cadherin was distinctively downregulated in the cell clones overexpressed PLK1 ,compared with those in the vector clones.This indicated that EMT occurred in ESCC cells.vimentin mRNA was also markedly in-creased.In the cell clones overexpressed PLK1 ,β-catenin were both elevated from the total cells and the nucleus.The expression of vimentin was reduced whenβ-catenin was knocked down.APC and GSK-3βwere both reduced from Axin immunoprecipitate in the cell clones overexpressed PLK1 .Conclusion PLK1 up-regulates vimentin and promotes EMT in ESCC cells probably by inhibiting the formation of protein degrada-tion complex and stabilizing β-catenin.
