Down-regulation of deoxycytidine kinase enhances acquired resistance to gemcitabine in pancreatic cancer

Seiji Ohhashi, Kenoki Ohuchida, Kazuhiro Mizumoto, Hayato Fujita, Takuya Egami, Jun Yu, Hiroki Toma, Shoko Sadatomi, Eishi Nagai, Masao Tanaka

研究成果: Contribution to journalArticle査読

78 被引用数 (Scopus)

抄録

Background: The functional roles of deoxycytidine kinase (dCK) in acquired resistance to gemcitabine remain unknown in pancreatic cancer. Here, the functional involvement of dCK in gemcitabine-resistance of pancreatic cancer was investigated. Materials and Methods: The levels of the dCK gene as well as other gemcitabine-related genes (hENT1, RRM1 and RRM2) were analyzed in gemcitabine-resistant pancreatic cancer cells (GR cells) using quantitative real-time reverse transcription polymerase chain reaction. The effects of inhibition of these genes on sensitivity to gemcitabine were evaluated. Results: In GR cells, expression of dCK was significantly reduced compared with that of parental cells (p<0.05). The dCK-targeting siRNA significantly reduced gemcitabine sensitivity (p<0.01) without affecting cell proliferation. The RRM1- and RRM2-targeting siRNAs increased gemcitabine sensitivity (p<0.05) and reduced cell proliferation even without gemcitabine treatment. The hENT-targeting siRNA did not affect gemcitabine sensitivity or cell proliferation. Conclusion: Down-regulation of dCK specifically enhanced acquired resistance to gemcitabine in pancreatic cancer cells without affecting their proliferation.

本文言語英語
ページ(範囲)2205-2212
ページ数8
ジャーナルAnticancer research
28
4 B
出版ステータス出版済み - 7 2008

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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