Title : Loss of protein kinase Cδ/HuR interaction is necessary to doxorubicin resistance in breast cancer cell lines.

Pub. Date : 2014 Apr

PMID : 24492650






4 Functional Relationships(s)
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1 This series of events is crucial to elicit the death pathway triggered by doxorubicin and is necessary to promote HuR function in post-transcriptional regulation of gene expression, because genetic ablation of PKCdelta caused the inability of HuR to bind its target mRNAs, topoisomerase IIalpha (TOP2A) included. Doxorubicin DNA topoisomerase II alpha Homo sapiens
2 In in vitro select doxorubicin-resistant human breast cancer cell lines upregulating the multidrug resistance marker ABCG2, PKCdelta, and HuR proteins were coordinately downregulated together with the doxorubicin target TOP2A protein whose mRNA was HuR-regulated. Doxorubicin DNA topoisomerase II alpha Homo sapiens
3 In in vitro select doxorubicin-resistant human breast cancer cell lines upregulating the multidrug resistance marker ABCG2, PKCdelta, and HuR proteins were coordinately downregulated together with the doxorubicin target TOP2A protein whose mRNA was HuR-regulated. Doxorubicin DNA topoisomerase II alpha Homo sapiens
4 Therefore, we show here that PKCdelta, HuR, and TOP2A constitute a network mediating doxorubicin efficacy in breast cancer cells. Doxorubicin DNA topoisomerase II alpha Homo sapiens