B4 androgen ablation: attacking the prostate cancer stem cell
Max S. Wicha
Max S. Wicha
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Commentary

B4 androgen ablation: attacking the prostate cancer stem cell

Abstract

There is increasing evidence that prostate cancers in rodent models and in men contain a cellular subpopulation that displays stem cell properties. These prostate cancer stem cells (PCSCs) lack androgen receptor expression and are increased in castration-resistant disease. In this issue of the JCI, a study from Yoshioka et al. demonstrates that PCSCs are regulated by a pathway in which α6β4 integrin amplifies signaling through ErbB2 and c-Met receptors. Targeting this pathway provides a novel therapeutic strategy for hormone refractory prostate cancer.

Authors

Max S. Wicha

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Figure 1

Regulation of CSC and bulk tumor cell population in prostate cancer.

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Regulation of CSC and bulk tumor cell population in prostate cancer. (A)...
(A) CSCs are regulated by androgen-independent pathways, involving α6β4 integrin that amplifies signaling through ErbB2 and c-Met pathways, which can be inhibited by lapatinib and crizotinib. (B) Bulk tumor cell growth is primarily regulated by androgens through interaction with AR and is sensitive to androgen blockade. Androgen signaling inhibits expression of Erbb2 and c-Met.