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Lambertianic acid exerts anticancer effects by inhibiting androgen reveptor (AR) signaling in LNCaP cells

Date

19 Dec 2015

Session

Poster presentation 1

Presenters

Myoung-Sun Lee

Citation

Annals of Oncology (2015) 26 (suppl_9): 71-79. 10.1093/annonc/mdv524

Authors

M. Lee1, S.O. Lee1, C.G. Kang2, E. Lee3, S. Kim2, H. Lee4

Author affiliations

  • 1 Cancer Preventive Material Development Research Center, Kyung Hee University, 130-701 - Seoul/KR
  • 2 Cancer Preventive Material Development Research Center, College Of Korean Medicine, Kyung Hee University, 130-701 - Seoul/KR
  • 3 College Of Korean Medicine, Kyung Hee University, Seoul/KR
  • 4 Cancer Preventive Material Development Research Center, Kyung Hee University, Seoul/KR
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Aim/Background

Prostate cancer (PCa) is a human male health concern in the whole world. Prostate cancer mediates proliferation through androgen receptor (AR) pathway. AR activity stimulates PSA expression in prostate cancer cells. The development of androgen dependent prostate cancer is generally thought to occur through mechanisms that regulate AR function. Lambertianic acid is known to exert anti-allergic and anti-bacterial effects. Recently, we have reported that Lambertianic acid (LA), a bioactive component of the Pinus Koraienesis, has anti-obesity effect.However,the anti cancer effects and mechanism of LA has not been studied.The goal of this study was to investigate the anti cancer mechanism of LA in LNCaP prostate cancer cells.

Methods

LNCaP cells were treated with LA or Mibolerone (Mib), and analyzed by western blotting, PSA secretion, luciferase activity of AR and PSA, crystal violet staining and cell cycle anlysis. The contribution of AR to anti-proliferation, anti-migration and apoptosis was assessed by siRNA-mediated AR knockdown. After AR silencing, expression of AR was observed by western blotting.

Results

LA inhibited AR protein levels as well as PSA both cellular and secretion levels in LNCaP cells. LA suppressed PSA and nuclear translocation of AR stimulated by a synthetic androgen (Mib). LA significantly decreased LNCaP cell proliferation and migration and induced G1 arrest. LA down-regulated CDK4/6 and cyclin D1, and activated p53 and its downstream p21 and p27. LA induced apoptosis, and increased apoptosis related proteins (cleaved cas-9 and 3, c-PARP and BAX), and inhibited bcl-2 expression. Further, the contribution of AR to LA induced anti-proliferation, anti-migration and apoptosis induction was assessed by AR siRNA.

Conclusions

Overall, our findings suggest that LA exerts anticancer activity via inhibition of AR pathway as a important therapeutic agent in androgen dependent prostate cancer.

Clinical trial identification

Disclosure

All authors have declared no conflicts of interest.

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