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

被引:24
|
作者
Dey, Heena [1 ]
Liu, Zhi-Ren [1 ]
机构
[1] Georgia State Univ, Dept Biol, Atlanta, GA 30303 USA
来源
BMC CELL BIOLOGY | 2012年 / 13卷
关键词
P68 RNA helicase; Oxaliplatin; Phosphorylation; p38 MAP kinase; DEAD-box; Apoptosis; ACTIVATED PROTEIN-KINASE; OVARIAN-CARCINOMA; HIV-1; ENVELOPE; PATHWAY; INDUCTION; GAMMA-H2AX; TRANSITION; MECHANISMS;
D O I
10.1186/1471-2121-13-27
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background: We previously demonstrated that p68 phosphorylation at threonine residues correlates with cancer cell apoptosis under the treatments of TNF-alpha 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.
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收藏
页数:8
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