Testosterone accumulation in prostate cancer cells is enhanced by facilitated diffusion.

ABSTRACT:

Background

Testosterone is a driver of prostate cancer (PC) growth via ligand-mediated activation of the androgen receptor (AR). Tumors that have escaped systemic androgen deprivation, castration-resistant prostate cancers (CRPC), have measurable intratumoral levels of testosterone, suggesting that a resistance mechanism still depends on androgen-simulated growth. However, AR activation requires an optimal intracellular concentration of androgens, a situation challenged by low circulating testosterone concentrations. Notably, PC cells may optimize their androgen levels by regulating the expression of steroid metabolism enzymes that convert androgen precursors into androgens. Here we propose that testosterone entry into the cell could be another control point.

Methods

To dete

SUBMITTER: Kaipainen A 

PROVIDER: S-EPMC6783279 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature