Sunday, November 15, 2020

Epigenetic modification‐dependent androgen receptor occupancy facilitates the ectopic TSPY1 expression in prostate cancer cell

Alexandros G.Sfakianakis shared this article with you from Inoreader
Μέσω Cancer Science

Summary

TSPY1 (testis‐specific protein Y‐encoded 1), a Y chromosome‐linked oncogene, is frequently activated in prostate cancers (PCa) and its expression is correlated with the poor prognosis of PCa. However, the cause leading to the ectopic transcription of TSPY1 in PCa is still unclear. Here, we observed that the methylation status in the CpG islands (CGIs) of the TSPY1 promoter was negatively correlated with its expression level in different human samples. The acetyl‐histone H4 and trimethylated histone H3‐lysine 4, two post translational modifications of histones, occupying on the TSPY1 promoter, faciliated the TSPY1 expression in PCa cells. Additionally, we found that androgen accelerated the TSPY1 trancription on condition of DNA demethylation of TSPY1‐CGIs and promoted PCa cell proliferation. Moreover, the binding of androgen receptor (AR) to the TSPY1 promoter, enhancing TSPY1 transcription, was detected in PCa cells. Taken together, our findings identify the regulation of DNA methylation, acting as a primary mechanism, on TSPY1 expression in PCa,and reveal that TSPY1 is an androgen‐AR axis‐regulated oncogene, suggesting a novel and potential target for PCa therapy

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