The androgen receptor can signal through Wnt/β-Catenin in prostate cancer cells as an adaptation mechanism to castration levels of androgens
2008

Androgen Receptor Signaling Through Wnt/β-Catenin in Prostate Cancer

publication Evidence: moderate

Author Information

Author(s): Schweizer Liang, Rizzo Cheryl A, Spires Thomas E, Platero J Suso, Wu Qiuyan, Lin Tai-An, Gottardis Marco M, Attar Ricardo M

Primary Institution: Bristol-Myers Squibb Company

Hypothesis

What effect does increased androgen receptor levels have on the Wnt signaling pathway in hormone-refractory prostate cancer cells?

Conclusion

The androgen receptor can promote Wnt signaling in prostate cancer cells, contributing to cell growth and malignancy at low androgen levels.

Supporting Evidence

  • AR overexpression enhances Wnt signaling activity in prostate cancer cells.
  • Physiological levels of androgen inhibit the growth-promoting effects of AR and Wnt signaling.
  • AR and β-Catenin co-localize in the nucleus of prostate cancer cells.
  • Wnt3A recruits AR to the promoter regions of Myc and Cyclin D1.
  • AR potentiates Wnt signaling at the chromatin level.

Takeaway

This study shows that the androgen receptor helps prostate cancer cells grow by working with another signaling pathway called Wnt, even when there are low levels of androgens.

Methodology

Transient transfections of human prostate cancer cell lines were performed to assess the interaction between androgen receptor and Wnt signaling.

Statistical Information

P-Value

p<0.005

Statistical Significance

p<0.005

Digital Object Identifier (DOI)

10.1186/1471-2121-9-4

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