Targeted silencing of TRPM7 ion channel induces replicative senescence and produces enhanced cytotoxicity with gemcitabine in pancreatic adenocarcinoma

Nelson Shu-Sang Yee, Weiqiang Zhou, Minsun Lee, Rosemary K. Yee

Research output: Contribution to journalArticle

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The transient receptor potential TRPM7 ion channel is required for cellular proliferation in pancreatic epithelia and adenocarcinoma. To elucidate the mechanism that mediates the function of TRPM7, we examined its role in survival of pancreatic cancer cells. RNA interference-mediated silencing of TRPM7 did not induce apoptotic cell death. TRPM7-deficient cells underwent replicative senescence with up-regulation of p16 CDKN2A and WRN mRNA. The combination of anti- TRPM7 siRNA and gemcitabine produced enhanced cytotoxicity as compared to gemcitabine alone. Thus, TRPM7 is required for preventing senescence, and modulation of TRPM7 expression may help improve treatment response of pancreatic cancer by combining with apoptosis-inducing agents.

Original languageEnglish (US)
Pages (from-to)99-105
Number of pages7
JournalCancer Letters
Issue number1
StatePublished - May 1 2012


All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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