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. Author manuscript; available in PMC: 2017 Nov 26.
Published in final edited form as: Biochem Biophys Res Commun. 2012 Nov 15;430(1):289–293. doi: 10.1016/j.bbrc.2012.10.135

Fig. 4.

Fig. 4

AR via the PIRH2-p53-p21 axis primes androgen-independent 104-R cells to UV-induced apoptosis. (A) and (B) 104-R cells were infected with lentiviruses encoding either AR shRNA or PIRH2 shRNA. Expression of PIRH2, AR, and p21 was analyzed by immunoblotting with corresponding antibodies (A). Apoptotic caspase assay (B). (C) Schematic illustration of how AR via the PIRH2-p53-p21 axis sensitizes androgen-independent prostate 104-R cancer cells to UV irradiation. AR promotes PIRH2-mediated p53 degradation, thereby reducing basal p21 expression. This will reduce the apoptotic threshold to UV-induced apoptosis.