Kartogenin Inhibits Prostate Cancer Cell Growth Through Smad2 Activation and Decreases Androgen Receptor Nuclear Localization.

Background/aim: De-differentiation is a key step for the progression of cancer cells. This study investigated the anti-tumor effect of kartogenin (KGN), which has the ability to differentiate cells, on prostate cancer (PC) cells.
Materials and Methods: The effects of KGN on androgen receptor (AR) nuclear localization, prostate-specific antigen (PSA) expression, and Smad2 activation as well as the growth of PC cell lines (LNCaP, 22Rv1 and PC-3) were analyzed.
Results: KGN significantly inhibited growth of AR-expressing LNCaP and 22Rv1 cells but not of AR-lacking PC-3 cells. KGN decreased AR nuclear localization and PSA expression, but did not enhance the anti-tumor effect of bicalutamide in LNCaP cells. KGN activated Smad2 both in the absence and presence of TGF-β1. KGN also inhibited growth of docetaxel-resistant PC cells, 22Rv1DR, and re-sensitized them to the agent.
Conclusion: KGN has a potential as a novel therapeutic for PC patients after treatment failure.
(Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)