Genomics

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LNCap cells treated with 3-diol; No_Tmt and 1, 3 and 6hrs after treatment


ABSTRACT: 5α-androstane-3α,17β-diol (3α-diol) is reduced from the potent androgen, 5α-dihydrotestosterone (5α-DHT), by reductive 3α-hydroxysteroid dehydrogenases (3α-HSDs). 3α-diol is believed to be a weak androgen, and has to be oxidized to 5α-DHT before it can exert its androgenic activity on androgen target tissues including the prostate. However, we repeatedly demonstrated that 3α-diol can be a potent androgen, activates cytoplasmic signaling pathway, and may be responsible for androgen-independent prostate cancer growth. A cancer-specific, cDNA-based membrane array was used to determine 3α-diol-mediated gene expressions in prostate cancer progression. Several canonical pathways appeared to be affected by 3α-diol-regulated signaling in LNCaP cells; among them are apoptosis signaling, PI3K/Akt signaling, and death receptor signaling pathways. Biological analysis of 3α-diol-activated signaling confirmed that 3α-diol augmented PI3K/Akt activation can be independent from the classical androgen receptor (AR) signaling. These observations sustained our previous report that 3α-diol continues to supported prostate cell survival and proliferation regardless the status of the AR. We provided the first global analysis of 3α-diol-activated gene expressions and identified cytoplasmic signaling pathways as important components of this response in human prostate cells. 3α-diol may play, therefore, a significant role for transition from androgen-dependent to androgen-independent prostate cancer progression in the presence of androgen blockade. Keywords: array, time course, androgen, prostate, cancer

ORGANISM(S): Homo sapiens

PROVIDER: GSE8860 | GEO | 2008/08/01

SECONDARY ACCESSION(S): PRJNA102219

REPOSITORIES: GEO

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