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• W2324156619 abstract "// Shumin Zhang 1, * , Lajos Gera 2, * , Kenza Mamouni 3 , Xin Li 3 , Zhengjia Chen 4 , Omer Kucuk 5 , Daqing Wu 1, 3, 6 1 Department of Urology, Emory University School of Medicine, Atlanta, GA, USA 2 Department of Biochemistry and Molecular Genetics, University of Colorado Denver, Anschutz Medical Campus, School of Medicine, Aurora, CO, USA 3 Department of Biochemistry and Molecular Biology, Medical College of Georgia and GRU Cancer Center, Augusta University, Augusta, GA, USA 4 Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, USA 5 Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, USA 6 MetCure Therapeutics LLC, Atlanta, GA, USA * These authors contributed equally to this work Correspondence to: Daqing Wu, email: dwu@gru.edu Keywords: prostate cancer, bone metastasis, survivin inhibitor, docetaxel resistance, preclinical models Received: January 07, 2016      Accepted: March 18, 2016      Published: March 30, 2016 ABSTRACT Bone metastasis is a major cause of prostate cancer (PCa) morbidity and mortality. Despite some success in transiently controlling clinical symptoms with docetaxel-based therapy, PCa patients become docetaxel-resistant and inevitably progress with no cure. We synthesized an acyl-tyrosine bisphosphonate amide derivative, BKM1644, with the intent of targeting bone metastatic PCa and enhancing docetaxel’s efficacy. BKM1644 exhibits potent anti-cancer activity in the NCI-60 panel and effectively inhibits the proliferation of metastatic, castration-resistant PCa (mCRPC) cells, with IC 50 ranging between 2.1 μM and 6.3 μM. Significantly, BKM1644 sensitizes mCRPC cells to docetaxel treatment. Mice with pre-established C4-2 tumors in the tibia show a marked decrease in serum prostate-specific antigen (control: 173.72 ± 37.52 ng/ml, combined treatment: 64.45 ± 22.19 ng/ml; p < 0.0001) and much improved bone architecture after treatment with the combined regimen. Mechanistic studies found that docetaxel temporarily but significantly increases survivin, an anti-apoptotic protein whose overexpression has been correlated with PCa bone metastasis and therapeutic resistance. Intriguingly, BKM1644 effectively inhibits survivin expression, which may antagonize docetaxel-induced survivin in bone metastatic PCa cells. Signal transducer and activator of transcription 3 (Stat3) may be involved in the suppression of survivin transcription by BKM1644, as confirmed by a survivin reporter assay. Collectively, these data indicate that BKM1644 could be a promising small-molecule agent to improve docetaxel efficacy and retard the bone metastatic growth of PCa." @default.
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• W2324156619 date "2016-03-30" @default.
• W2324156619 modified "2023-10-18" @default.
• W2324156619 title "Inhibition of skeletal growth of human prostate cancer by the combination of docetaxel and BKM1644: an aminobisphosphonate derivative" @default.
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• W2324156619 doi "https://doi.org/10.18632/oncotarget.8481" @default.
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