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Open Access Research article

Phosphorylation of P68 RNA Helicase by P38 MAP kinase contributes to colon cancer cells apoptosis induced by oxaliplatin

Heena Dey and Zhi-Ren Liu*

Author Affiliations

Department of Biology, Georgia State University, Atlanta, GA 30303, USA

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BMC Cell Biology 2012, 13:27  doi:10.1186/1471-2121-13-27

Published: 31 October 2012

Abstract

Background

We previously demonstrated that p68 phosphorylation at threonine residues correlates with cancer cell apoptosis under the treatments of TNF-α and TRAIL (Yang, L. Mol Cancer Res Vol 3, pp 355–63 2005).

Results

In this report, we characterized the role of p68 phosphorylation in apoptosis induction under the treatment of oxaliplatin in the colon cancer cells. Our data suggest that oxaliplatin treatment activates p38 MAP kinase, which subsequently phosphorylates p68 at T564 and/or T446. The phosphorylation of p68, at least partially, mediates the effects of the drug on apoptosis induction, as mutations at these two sites greatly reduce the cancer cell death.

Conclusion

Our studies reveal an important molecular mechanism that mediates the effects of anti-cancer drug, providing a potential strategy for improving cancer treatment.

Keywords:
P68 RNA helicase; Oxaliplatin; Phosphorylation; p38 MAP kinase; DEAD-box; Apoptosis