Title : Modulation of Rad51, ERCC1, and thymidine phosphorylase by emodin result in synergistic cytotoxic effect in combination with capecitabine.

Pub. Date : 2011 Mar 1

PMID : 21168393






6 Functional Relationships(s)
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1 Modulation of Rad51, ERCC1, and thymidine phosphorylase by emodin result in synergistic cytotoxic effect in combination with capecitabine. Capecitabine RAD51 recombinase Homo sapiens
2 Accordingly, we aimed to explore the molecular mechanism of emodin enhances the capecitabine-induced cytotoxicity through controlling Rad51, ERCC1, and TP expression in human non-small cell lung cancer (NSCLC). Capecitabine RAD51 recombinase Homo sapiens
3 The results show that capecitabine increases the phosphorylation of MKK1/2-ERK1/2 and protein levels of Rad51 and ERCC1 through enhancing the protein stability. Capecitabine RAD51 recombinase Homo sapiens
4 Depletion of endogenous Rad51 or ERCC1 expression by specific small interfering RNA transfection significantly increases capecitabine-induced cell death and growth inhibition. Capecitabine RAD51 recombinase Homo sapiens
5 Emodin enhances the capecitabine-induced cytotoxic effects through ERK1/2 inactivation and decreasing the Rad51 and ERCC1 protein levels induced by capecitabine. Capecitabine RAD51 recombinase Homo sapiens
6 We conclude that enhancing the cytotoxicity to capecitabine by emodin is mediated by down-regulation the expression of Rad51 and ERCC1 and up-regulation TP expression. Capecitabine RAD51 recombinase Homo sapiens