Kartogenin inhibits prostate cancer cell growth through Smad2 activation and decreases androgen receptor nuclear localization

Manabu Takai, Kyojiro Kawakami, Yasunori Fujita, Taku Kato, Daiki Kato, Koji Iinuma, Takuya Koie, Masafumi Ito, Kosuke Mizutani

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)4753-4759
Number of pages7
JournalAnticancer research
Volume41
Issue number10
DOIs
Publication statusPublished - 10-2021
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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