Abstract
Abstract : Mutations have been recently identified in the EphB2 receptor gene in prostate cancer suggesting that EphB2, a member of the large Eph receptor tyrosine kinase family, is a tumor suppressor in prostate cancer. Consistent with a tumor suppressor activity, we found that EphB2 is more highly expressed in non-transformed BPH-1 prostate epithelial cells than in several prostate cancer cell lines. Furthermore, EphB2 expression was rapidly lost in stably transfected DU145 prostate cancer cells, suggesting that EphB2 inhibits cell growth and/or survival. We plan to further examine the effects of EphB2 signaling on the behavior of cancer cells in tissue culture and on prostate cancer progression in a mouse xenograft model. We will also examine whether other Eph receptors that we have detected in prostate cancer cells have effects similar to EphB2. The information obtained from these studies will help guide the design of appropriate treatment strategies and determine if prostate cancers should be screened for Eph receptor and ephrin ligand expression for prognostic purposes.
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