TY - JOUR
T1 - Kartogenin inhibits prostate cancer cell growth through Smad2 activation and decreases androgen receptor nuclear localization
AU - Takai, Manabu
AU - Kawakami, Kyojiro
AU - Fujita, Yasunori
AU - Kato, Taku
AU - Kato, Daiki
AU - Iinuma, Koji
AU - Koie, Takuya
AU - Ito, Masafumi
AU - Mizutani, Kosuke
N1 - Funding Information:
This work was partially supported by Japan Society for the Promotion of Science, KAKENHI Grant Number 21K09340. The Authors are grateful to Ayako Nagasawa for her invaluable contributions to data acquisition.
Publisher Copyright:
© 2021 International Institute of Anticancer Research. All rights reserved.
PY - 2021/10
Y1 - 2021/10
N2 - 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.
AB - 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.
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U2 - 10.21873/anticanres.15290
DO - 10.21873/anticanres.15290
M3 - Article
C2 - 34593424
AN - SCOPUS:85116494199
SN - 0250-7005
VL - 41
SP - 4753
EP - 4759
JO - Anticancer Research
JF - Anticancer Research
IS - 10
ER -