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• W1230611947 startingPage "1064" @default.
• W1230611947 abstract "The mechanisms that regulate hematopoietic stem cell (HSC) dormancy and self-renewal are well established and are largely dependent on signals emanating from the HSC niche. Recently, we found that prostate cancer (PCa) cells target the HSC niche in mouse bone marrow (BM) during metastasis. Little is known, however, as to how the HSC niche may regulate dormancy in cancer cells. In this study, we investigated the effects of TANK binding kinase 1 (TBK1) on PCa dormancy in the BM niche. We found that binding with niche osteoblasts induces the expression of TBK1 in PCa cells PC3 and C4-2B. Interestingly, TBK1 interacts with mammalian target of rapamycin (mTOR) and inhibits its function. Rapamycin, an mTOR inhibitor, induces cell cycle arrest of PCa cells and enhances chemotherapeutic resistance of PCa cells. As a result, the knockdown of TBK1 decreases PCa stem-like cells and drug resistance in vitro and in vivo. Taken together, these results strongly indicate that TBK1 plays an important role in the dormancy and drug resistance of PCa." @default.
• W1230611947 created "2016-06-24" @default.
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• W1230611947 date "2013-09-01" @default.
• W1230611947 modified "2023-10-12" @default.
• W1230611947 title "TBK1 Regulates Prostate Cancer Dormancy through mTOR Inhibition" @default.
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• W1230611947 doi "https://doi.org/10.1593/neo.13402" @default.
• W1230611947 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3769885" @default.
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