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(American Journal of Pathology. 1999;154:1503-1512.)
© 1999 American Society for Investigative Pathology

Regular Articles

Distinct CXC Chemokines Mediate Tumorigenicity of Prostate Cancer Cells

Bethany B. Moore*, Douglas A. Arenberg*, Kevin Stoy{dagger}, Tamara Morgan{dagger}, Christina L. Addison*, Susan B. Morris*, Mary Glass*, Carol Wilke*, Ying Ying Xue*, Stephanie Sitterding*, Steven L. Kunkel{ddagger}, Marie D. Burdick* and Robert M. Strieter*

From the Departments of Internal Medicine*
and Pathology{ddagger}
and the Undergraduate Research Opportunities Program,{dagger}
University of Michigan Medical Center, Ann Arbor, Michigan

Prostate cancer is the second leading cause of malignancy-related mortality in males in the United States. As a solid tumor, clinically significant tumor growth and metastasis are dependent on nutrients and oxygen supplied by tumor-associated neovasculature. As such, there is a selective tumorigenic advantage for those neoplasms that can produce angiogenic mediators. We show here that human prostate cancer cell lines can constitutively produce angiogenic CXC chemokines. Tumorigenesis of PC-3 prostate cancer cells was shown to be attributable, in part, to the production of the angiogenic CXC chemokine, interleukin (IL)-8. Neutralizing antisera to IL-8 inhibits PC-3 tumor growth in a human prostate cancer/SCID mouse model. Furthermore, angiogenic activity in PC-3 tumor homogenates was attributable to IL-8. In contrast, the Du145 prostate cancer cell line uses a different angiogenic CXC chemokine, GRO-{alpha}, to mediate tumorigenicity. Neutralizing antisera to GRO-{alpha} but not IL-8 reduced tumor growth in vivo and reduced the angiogenic activity in tumor homogenates. Thus, prostate cancer cell lines can use distinct CXC chemokines to mediate their tumorigenicity.




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