期刊
JOURNAL OF MOLECULAR ENDOCRINOLOGY
卷 37, 期 2, 页码 283-300出版社
SOC ENDOCRINOLOGY
DOI: 10.1677/jme.1.02062
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资金
- NCI NIH HHS [CA16672] Funding Source: Medline
- NIDDK NIH HHS [1R01 DK065156 01] Funding Source: Medline
Various cofactors have been shown to regulate androgen receptor (AR) transactivation, but their physiological functions in the AR pathway and prostate turnorigenesis are undefined. Here, we found that AR cofactor (p44) translocation from the nucleus to the cytoplasm in prostate epithelial cells (ECs) is associated with prostate tumorigenesis. The forced nuclear localization of p44 inhibited prostate cancer cell growth by G1 cell-cycle arrest. Consistently, mice lacking one allele of the p44 gene developed prostatic hyperplasia. Therefore, p44 is required for proper expression of AR-target genes to maintain the differentiation of prostate ECs, and p44 translocation from the nucleus into the cytoplasm in prostate cancer cells or loss of one allele in mouse results in excessive prostate EC proliferation.
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