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. 2016 Oct 10;8(2):3724–3745. doi: 10.18632/oncotarget.12554

Figure 1. Molecular mechanisms driving CRPC.

Figure 1

Development of CRPC has been attributed to numerous potential molecular mechanisms, including: 1) somatic mutations of AR resulting in increased affinity for ligands; 2) amplification of the AR gene locus; 3) intracrine biosynthesis of androgens in prostate cancer cells from adrenal steroids and cholesterol; 4) expression of constitutively active, ligand-independent AR splice variants; 5) non-canonical activation of AR by protein kinase signaling pathways in the absence of ligand by receptor tyrosine kinases (RTK); 6) AR-independent mechanisms operating outside of the AR signaling axis which promote castrate-resistant growth of prostate cancer.