A novel group of genes regulates susceptibility to antineoplastic drugs in highly tumorigenic breast cancer cells.

摘要: Doxorubicin is an anthracycline antibiotic used for cancer chemotherapy. The utility of doxorubicin limited by its inability to kill all the cells within a tumor and resistant emerging from treated population. We have screened genes that regulate susceptibility in highly tumorigenic breast cDNA microarray RNA interference (RNAi) analysis, we identified associated with both proliferation cell cycle arrest after treatment. confirmed MDA-MB-231 induce expression carbonic anhydrase II (CAII), inhibitor differentiation/DNA binding 2 (Id2), activating transcription factor 3 (Atf3), phosphatidylinositol 3-kinase 55-kDa regulatory subunit p55PIK. These were induced at different times varying specificities chemotherapeutic drugs. In addition being transcriptional level, CAII clusterin proteins elevated CAII, Id2, p55PIK, not altered MCF-7 cells, weakly line previous studies doxorubicin-regulated gene expression. By inhibiting using RNAi, found increase survival treatment, whereas Id2 increases doxorubicin. Our results support model which response distinct less malignant cells. drug positively negatively may be novel targets therapeutic intervention.