Differential expression of interleukin-8 and its receptors in the neuroendocrine and non-neuroendocrine compartments of prostate cancer.

Journal Article (Journal Article)

Hormonal therapy (androgen ablation and/or inhibition of androgen action) is the treatment of choice for advanced prostate cancer. After an initial response in most patients, tumors invariably progress to an androgen-independent state. It is unclear how prostate cancer cells proliferate without androgen. Recent studies suggest that interleukin-8 may promote androgen-independent proliferation, but the source of interleukin-8 in the prostate is unknown. Using immunohistochemistry, we show that interleukin-8 was expressed by the neuroendocrine tumor cells in human prostate cancer tissue. Expression of the interleukin-8 receptor CXCR1 was negative or low in benign prostatic tissue and was frequently increased in malignant cells of high-grade prostatic intraepithelial neoplasia and prostate cancer; however, CXCR1 was not detected in the neuroendocrine tumor cells, suggesting a paracrine mechanism by which interleukin-8 produced by neuroendocrine tumor cells stimulates androgen-independent proliferation of prostate cancer. Neuroendocrine tumor cells expressed another type of interleukin-8 receptor, CXCR2, suggesting an autocrine mechanism by which interleukin-8 regulates the differentiation or function of the neuroendocrine cells. These results, combined with previous reports that neuroendocrine differentiation is induced by hormonal therapy, suggest that neuroendocrine cells play an important role in promoting androgen-independent growth of prostate cancer through interleukin-8 signaling.

Full Text

Duke Authors

Cited Authors

  • Huang, J; Yao, JL; Zhang, L; Bourne, PA; Quinn, AM; di Sant'Agnese, PA; Reeder, JE

Published Date

  • June 2005

Published In

Volume / Issue

  • 166 / 6

Start / End Page

  • 1807 - 1815

PubMed ID

  • 15920165

Pubmed Central ID

  • PMC1602414

International Standard Serial Number (ISSN)

  • 0002-9440

Digital Object Identifier (DOI)

  • 10.1016/S0002-9440(10)62490-X

Language

  • eng

Conference Location

  • United States