Simultaneous inhibition of XIAP and survivin expression on EMT and invasion of human pancreatic cancer cells.
- Author:
Hongyan ZAI
1
;
Xiaoping YI
;
Yixiong LI
;
Chun JIANG
;
Xinsheng LU
Author Information
1. Department of Gerneral Surgery, Xiangya Hospital, Central South University, Changsha, China.
- Publication Type:Journal Article
- MeSH:
Antigens, CD;
Cadherins;
metabolism;
Cell Line, Tumor;
Cell Movement;
Epithelial-Mesenchymal Transition;
genetics;
Humans;
Inhibitor of Apoptosis Proteins;
genetics;
metabolism;
Neoplasm Invasiveness;
PTEN Phosphohydrolase;
metabolism;
Pancreatic Neoplasms;
pathology;
Proto-Oncogene Proteins c-akt;
metabolism;
Signal Transduction;
Snail Family Transcription Factors;
Survivin;
Transcription Factors;
metabolism;
X-Linked Inhibitor of Apoptosis Protein;
genetics;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2012;37(9):883-888
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the simultaneous inhibition of X-linked inhibitor of apoptosis protein (XIAP) and survivin expression on epithelial-mesenchymal transition (EMT) and invasiion of pancreatic cancer cells Panc-1, and its mechanism.
METHODS:On the established human pancreatic cancer cells Panc-1-XS, the expression of XIAP and survivin was inhibited simultaneously. Cell invasion and migration were detected by Transwell chamber experiments and scratch test, and the expression of epithelial marker E-cadherin, mesenchymal markers Slug, phosphatase and tensin homolog deleted on chromosome ten (PTEN) and P-Akt protein was determined by Western blot.
RESULTS:Cell invasion and migration of Panc-1-XS cells decreased significantly, accompanied by significantly upregulated protein expression of E-cadherin, and significantly declined protein expression of the Slug, indicating increased mesenchymal-epithelial conversion (MET); and increased protein expression of PTEN, and declined protein expression of P-Akt.
CONCLUSION:Simultaneously inhibiting the expression of XIAP and survivin can partially reverse EMT phenotype of pancreatic cancer Panc-1 cells, which then significantly reduces the cell invasion and migration of Panc-1 cell lines. This process may be regulated by PTEN/PI3K/Akt signaling pathway.
