Article

The survivin suppressant YM155 potentiates chemosensitivity to gemcitabine in the human pancreatic cancer cell line MiaPaCa-2.

Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Anticancer research (impact factor: 1.73). 05/2012; 32(5):1681-8. pp.1681-8
Source: PubMed

ABSTRACT Survivin is a negative regulator of apoptosis. We evaluated the efficacy of YM155, a selective suppressant of survivin, in combination with gemcitabine in the pancreatic cancer cell line MiaPaCa-2.
Expression of survivin was demonstrated by immunoblotting. Cell cycle progression was determined by flow cytometric analysis. Cell viability was assayed using the trypan blue exclusion assay.
Gemcitabine up-regulated survivin expression, whereas treatment with YM155 suppressed the expression of survivin. Concomitant treatment with YM155 enhanced chemosensitivity to gemcitabine, which was accompanied by a decrease in the expression of survivin. Knockdown of endogenous survivin via RNA interference also enhanced the sensitivity to gemcitabine. In addition, YM155 potentiated the antitumor effect of gemcitabine in xenograft tumors of MiaPaCa-2.
YM155 potentiates chemosensitivity to gemcitabine in pancreatic cancer cells by suppressing the induction of survivin. Combination treatment with gemcitabine and YM155 may be a potential therapeutic strategy for the treatment of pancreatic cancer that warrants further clinical investigation.

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Keywords

antitumor effect
 
Cell cycle progression
 
Cell viability
 
Combination treatment
 
efficacy
 
endogenous survivin
 
flow cytometric analysis
 
gemcitabine
 
Gemcitabine up-regulated survivin expression
 
negative regulator
 
pancreatic cancer
 
pancreatic cancer cell line MiaPaCa-2
 
pancreatic cancer cells
 
potential therapeutic strategy
 
RNA interference
 
selective suppressant
 
Survivin
 
trypan blue exclusion assay
 
YM155 potentiates chemosensitivity
 
YM155 suppressed
 

Dok Hyun Yoon