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

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


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
Issue number1-3
StatePublished - May 8 2002
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by the Ministry of Science and Technology, South Korea, and the KOSEF through the Research Center for Proteineous Materials. We thank Dr. D. Mercola (ISIS Pharmaceuticals, Carlsbad, CA, USA) for kindly providing us antisense oligonucleotides to JNK1 and JNK2 and scrambled oligonucleotide.


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


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