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- W3199882008 abstract "Despite the fact that androgen deprivation therapy(ADT) with various antiandrogens can effectively reduce tumor sizeand delay the occurrence of the castration resistant stage inadvanced prostate cancer (PCa), its effect on PCa metastasisremains unclear and PCa-related deaths continually increase.Besides the signaling changes in PCa cells, increasing evidencesuggest that ADT induced inflammation in the PCa microenvironmentmay contribute to cancer progression and metastasis. We examinedPCa patients treated with ADT for tumor growth and metastasis andfound that in some PCa patients their primary tumors are reducedwith corresponding decreases in PSA values, yet metastasisincreased. Using various in vitro invasion assays in 4 differenthuman PCa cell lines and in the in vivo xenograft metastasis micemodels, we evaluated the effects of ADT with the currently usedanti-androgens (Casodex® and MDV3100) and the newly developedanti-androgen receptor (AR) compounds (ASC-J9® andcryptotanshinone) on PCa cell growth and invasion. In vitroresults are consistent with these human clinical results showingthat 10 μM Casodex® or MDV3100 could suppress PCa cell growth andreduce PSA, yet significantly enhance PCa invasion in all 4 PCacell lines tested. Mechanism dissection indicated theseantiandrogens might enhance the TGF-β→Smad3→MMP-9 pathway. Incontrast, newly developed anti-AR compounds, such as ASC-J9® andcryptotanshinone, showed promising effects on both anti-growth andanti-invasion via down-regulation of MMP9 expression in both invitro cells and in vivo mouse model. Using the in vitroPCa/macrophage co-culture system in both human (C4- 2B/THP-1) andmouse (TRAMP-C1/RAW264.7) models, we found that ADT can enhancethe PCa metastasis via the regulation of macrophage recruitment byCCL2 expression. Meanwhile, ASC-J9® inhibited both macrophagemigration and PCa invasion via the inhibition of STAT3 activationand CCL2 expression through an ARindependent pathway. Theorthotopic implantation of TRAMP-C1 cells into nude mice modelprovided further in vivo evidence that ADT induced PCa metastasisvia upregulation of STAT3/CCL2 in the tumor micro-environment.Our findings pointed out the potential risk of the currently usedanti-androgens for their un-recognized and un-desired effects onenhancing PCa metastasis in some selective patients and provide anovel strategy with newly developed anti-AR compounds to targetboth PCa growth and invasion to battle metastatic castrationresistant PCa. Keywords: prostate cancer, anti-androgen, Akt,TGF-β, macrophage, CCL2, invasion, ASC-J9®, Cryptotanshinone,Casodex®, and MDV3100." @default.
- W3199882008 created "2021-09-27" @default.
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- W3199882008 date "2013-01-01" @default.
- W3199882008 modified "2023-09-27" @default.
- W3199882008 title "Differential Androgen Deprivation Therapies Promote orSuppress Prostate Cancer Metastasis" @default.
- W3199882008 hasPublicationYear "2013" @default.
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