Overexpression of Aldo-Keto Reductase 1C3 in LNCaP Cells Diverts Androgen Metabolism Towards Testosterone Resulting in Resistance to the 5α-Reductase Inhibitor Finasteride
January 2012
in “
The Journal of Steroid Biochemistry and Molecular Biology
”
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Studysummary This study found that overexpression of AKR1C3 in prostate cancer cells redirected androgen metabolism towards testosterone production, which facilitated cell proliferation, potentially reducing the effectiveness of finasteride treatment. Our plain-language summary of this paper — not a Tressless recommendation.
The study found that overexpression of the enzyme AKR1C3 in LNCaP cells led to a diversion of androgen metabolism towards testosterone, resulting in resistance to the 5α-reductase inhibitor finasteride. This was due to AKR1C3 redirecting A4-Adione metabolism towards testosterone production, leading to increased levels of testosterone and decreased sensitivity to finasteride. The study suggests that inhibition of AKR1C3 could prevent the conversion of A4-Adione to testosterone and the conversion of 5a-androstane-3,17-dione to 5a-DHT, which are potent ligands for the AR, and could have therapeutic consequences for the use of inhibitors that target 5α-reductase in prostate cancer.
