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- W2896804927 abstract "4517 Acquisition of resistance to androgen ablation therapy by prostate tumors during androgen deprivation remains a major obstacle to the effective treatment of prostate cancer. One of the reasons for development of androgen-independent prostate tumors following anti-androgen therapy is abnormal functioning of the androgen receptor (AR) as a nuclear receptor. The complexity of androgen-mediated regulation of gene transcription is developed from the ability of the AR to modulate transcription of a variety of genes through activation or inactivation of a number of transcription factors. To identify transcription factors that are activated or inactivated in response to androgen treatment or deprivation, we used human xenograft prostate tumors at different stages of androgen sensitivity or refractoriness. We used a novel protein-DNA interaction based method, TranSignal protein-DNA array, to profile activation status of transcription factors. We used crude nuclear extracts of five human prostate xenograft CWR22 tumors and a prostate cancer cell line to monitor the binding ability of transcription factors to specific response elements upon activation from a pool of 54 unique transcription factor binding sequences. Various CWR22 tumors include tumors from a) intact mice (Ctr), b) from castrated mice (Cstr), c) from castrated mice with androgen pellets implanted (CstrA), d) mice injected with androgen-independent human tumor cells (R), and e) mice exhibiting relapsed tumors after castration (RUI). We also used PC3AR cells, a stably transfected PC3 cell line capable of expressing androgen receptor and PSA, with or without treatment with DHT. Our studies using CWR22 human prostate cancer xenograft tumors showed differential activation of a number of transcription factors between tumors from castrated and androgen supplemented castrates. This includes AP-2 (1), CREB, E2F, GATA-1-binding protein, GRE, NF-1, NFATc, NF-E1, NF-E2, NFkB, Pit1, Sp1, TRDR4 and USF-1 transcription factors following androgen treatment. Direct binding of some of the transcription factors to their cognate response elements are validated by electrophoretic mobility shift assays. The overall pattern of the response element occupancy indicates a higher number of transcription factors are DNA-bound in Ctr, CstrA and RUI tumors compared to the Cstr tumor, which suggests possible induction of transcription of specific genes involved in progression of tumor growth in response to androgen. Increased activation of transcription factors in RUI tumors, whereas, reflects possible onset of an androgen-independent mechanism mediated by either AR or through an AR bypass mechanism." @default.
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- W2896804927 date "2005-05-01" @default.
- W2896804927 modified "2023-09-23" @default.
- W2896804927 title "Profiling of transcription factor activation by androgen receptor in androgen dependent and androgen independent xenograft prostate tumors" @default.
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