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. 2017 May 18;8(27):44447–44464. doi: 10.18632/oncotarget.17968

Figure 4. Hyper-induction of CYP24A1 limits the 1,25D(OH)2D3 but not the VDRM2-dependent actions of VDR.

Figure 4

The presence of the TMPRSS2:ERG fusion gene leads to high basal levels of ERG that cooperate with activated VDR to hyper-induce CYP24A1 expression in VCaP cells. (A) 1,25D(OH)2D3 (1,25D) is a substrate for CYP24A1 and 1,25D(OH)2D3-dependent VDR activity is reduced after incubation with VCaP cells. (B) VDRM2 is not predicted to be a substrate for CYP24A1 and VDRM2-dependent VDR activity is sustained after incubation with VCaP cells. VDRE: Vitamin D response element, EBS: Ets binding site.