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• W2034800705 abstract "Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FLTaxane compounds, such as docetaxel and paclitaxel, are microtubule-targeted tubulin-polymerizing agents and have proven to be the first line of treatment choice for castration-resistant prostate cancer and tamoxifen-resistant breast cancer cells. However resistance to taxane compounds develops commonly due to altered beta tubulin isotypes or development of multidrug resistance (MDR) through activation of p-glycoprotein drug efflux pump. In addition there are serious side effects and systemic toxicity encountered with docetaxel treatment. There is a need to enhance the efficacy of the taxane compounds by identifying novel targets, inhibition of which would induce mitotic arrest and apoptosis. LIM kinase1 (LIMK1) is a serine/threonine kinase, which coordinates microtubule stability and reorganization of actin cytoskleton through inactivating phosphorylation of cofilin, and is involved in regulation of the mitotic process. LIMK1 is overexpressed in breast and prostate tumors and in breast and prostate cancer cells in culture. Ectopic expression of LIMK1 promotes altered cell cycle progression and mitotic defects. Furthermore, LIMK1 expression prevents normal cellular response to paclitaxel in prostate epithelial cells, such as metaphase arrest and retarded cell growth. In this study, we show that ectopic expression of LIMK1 in BPH-1 cells decreased cytotoxic effects of paclitaxel through reduction of the number of apoptotic cells. Cell viability analysis using MTT assay showed that LIMK1 expressing cells maintained a higher viable cell density compared to control cells following paclitaxel treatment. LIMK1 expression in BPH-1 cells also increased BCL2 expression and decreased translocation of BAX to mitochondria compared to control cells. siRNA-induced down regulation of LIMK1 expression increased docetaxel sensitivity of breast and prostate cancer cells. Flow cytometric analysis of LIMK1 siRNA treated cells showed increased percentage of apoptotic cells compared to control RNA treated cells. Western blot analysis showed increased cleavage of apoptotic markers PARP, caspase 3 and caspase 9 in LIMK1 shRNA transfected prostate cancer cells upon docetaxel treatment compared to cells transfected with scrambled shRNA. Our study suggests that targeted inhibition of LIMK1 expression may potentiate the effects of taxane compounds on breast and prostate cancer cells. This study will have a broad impact on management of castration-resistant prostate and tamoxifen-resistant/ER-apha negative breast cancer cells with increased sensitivity of taxane compounds at a lower dose and hence less systemic toxicity, which could be applicable to other types of cancers as well.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3613. doi:10.1158/1538-7445.AM2011-3613" @default.
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• W2034800705 date "2011-04-15" @default.
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• W2034800705 title "Abstract 3613: Down regulation of LIM kinase1 enhances taxane sensitivity of cancer cells" @default.
• W2034800705 doi "https://doi.org/10.1158/1538-7445.am2011-3613" @default.
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