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. 2014 Jun 18;289(30):20824–20835. doi: 10.1074/jbc.M114.559518

FIGURE 7.

FIGURE 7.

H2S inhibits AR dimerization. A, H2S attenuated AR dimer formation in LNCaP cells. The cells were incubated with or without R1881 (10 nm) and/or NaHS (30 μm) for 48 h. *, p < 0.05 versus R1881 group and NaHS group; #, p < 0.05 versus R1881 group. B, H2S inhibited AR dimerization in Cos-1 cells. Twenty-four hours after the cells were transfected with wild-type AR plasmid, R1881 (10 nm) and/or NaHS (30 μm) were added for another 48 h. *, p < 0.05 versus R1881 group and NaHS group; #, p < 0.05 versus R1881 group. C, mutation of C611/614 eliminated H2S-induced AR dimerization inhibition. Twenty-four hours after the cells were transfected with AR mutants, R1881 (10 nm) and/or NaHS (30 μm) were added for another 48 h. *, p < 0.05 versus R1881 group. D and E, AR overexpression abolished the antigrowth effect of H2S on prostate cancer cells. LNCaP cells were transfected with wild-type AR in the presence or absence of NaHS (30 μm) for 48 h. The experiments were repeated at least three times. Data are presented as means ± S.E.