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

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...

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Detalles Bibliográficos
Autores principales: Dey, Heena, Liu, Zhi-Ren
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519718/
https://www.ncbi.nlm.nih.gov/pubmed/23110695
http://dx.doi.org/10.1186/1471-2121-13-27
Descripción
Sumario: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.