Human pancreatic cancer cells with acquired gemcitabine resistance exhibit significant up-regulation of peroxiredoxin-2 compared to sensitive parental cells

Shigeyuki Suenaga, Yasuhiro Kuramitsu, Yufeng Wang, Byron Baron, Takao Kitagawa, Junko Akada, Kazuhiro Tokuda, Seiji Kaino, Shin Ichiro Maehara, Yoshihiko Maehara, Isao Sakaida, Kazuyuki Nakamura

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)

Abstract

Gemcitabine (2′-deoxy-2′-difluorodeoxycytidine) is the only clinically effective drug for pancreatic cancer. However, high levels of inherent and acquired tumor resistance to gemcitabine lead to difficulty of chemotherapy for pancreatic cancer. We have reported on a proteomic study of gemcitabine-sensitive KLM1 and -resistant KLM1-R pancreatic cancer cells, and identified some proteins which were shown to be up-regulated in KLM1-R compared to KLM1 cells. In those proteomic studies, peroxiredoxin-2 was listed as an up-regulated protein in KLM1-R cells. Peroxiredoxin-2 is a member of a family of peroxiredoxins providing a protective role for redox damage. In this study, the expression of peroxiredoxin-2 in KLM1 and KLM1-R cells was compared. It was found that peroxiredoxin-2 was significantly up-regulated in KLM1-R cells compared to KLM1 cells (p<0.001). However, peroxiredoxin-1 expression was significantly down-regulated in KLM1-R cells (p<0.001). These results suggest that peroxiredoxin-2 is a possible candidate biomarker for predicting the response of patients with pancreatic cancer to treatment with gemcitabine.

Original languageEnglish
Pages (from-to)4821-4826
Number of pages6
JournalAnticancer research
Volume33
Issue number11
Publication statusPublished - Nov 2013

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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