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

Dok Hyun Yoon, Jae Sik Shin, Dong Hoon Jin, Seung Woo Hong, Kyung A. Jung, Seung Mi Kim, Yong Sang Hong, Kyu Pyo Kim, Jae Lyun Lee, Cheolwon Suh, Jung Shin Lee, Tae Won Kim

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

Background: 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. Materials and Methods: 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. Results: Gemcitabine upregulated 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. Conclusion: 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.

Original languageEnglish (US)
Pages (from-to)1681-1688
Number of pages8
JournalAnticancer Research
Volume32
Issue number5
StatePublished - May 1 2012

Keywords

  • Gemcitabine
  • In vivo model
  • MiaPaCa-2
  • Pancreatic cancer
  • Survivin
  • Xenograft
  • YM155

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