Rac1 prevents cisplatin-induced apoptosis through down-regulation of p38 activation in NIH3T3 cells

Hye Gwang Jeong, Hyun Ju Cho, In Youb Chang, Sang Pil Yoon, Young Jin Jeon, Myung Hee Chung, Ho Jin You

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Abstract

In this study, the role of V12-Rac1 in the cisplatin-induced apoptosis was investigated. Cisplatin-induced apoptosis is associated with cytochrome c release, which can be inhibited by V12-Rac1 expression. The analysis of mitogen-activated protein kinase activity indicated that V12-Rac1 expression led to a decrease in p38 activity after exposure to cisplatin but not c-jun N-terminal kinase and extracellular signal-regulated kinase. Using pharmacological inhibitors, it was found that only p38 is a critical mediator in the cisplatin-induced apoptosis of NIH3T3 cells. This suggests that V12-Rac1 can stimulate the anti-apoptotic signaling pathway in response to cisplatin, and that decreased p38 activity caused by V12-Rac1 expression in cisplatin-treated NIH3T3 cells is crucial for V12-Rac1-dependent cell survival.

Original languageEnglish (US)
Pages (from-to)129-134
Number of pages6
JournalFEBS Letters
Volume518
Issue number1-3
DOIs
StatePublished - May 8 2002

Keywords

  • Apoptosis
  • Cisplatin
  • Cytochrome c
  • Rac1
  • Rho family
  • p38

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    Jeong, H. G., Cho, H. J., Chang, I. Y., Yoon, S. P., Jeon, Y. J., Chung, M. H., & You, H. J. (2002). Rac1 prevents cisplatin-induced apoptosis through down-regulation of p38 activation in NIH3T3 cells. FEBS Letters, 518(1-3), 129-134. https://doi.org/10.1016/S0014-5793(02)02674-1