Differential expression and/or activation of P38MAPK, erk1/2, and jnk during the initiation and progression of prostate cancer.

Background: Members of the mitogen-activated protein kinase (MAPK) family are capable of transducing signals from a wide variety of stimuli, including growth factors, G-protein coupled receptors, and cytokines that are likely to play a role in the initiation and/or progression of prostate cancer.

Methods: The expression and activation of three members of the MAPK family, namely, erk, jnk, and p38MAPK was examined using Western blotting and immunohistochemistry during tumor progression in a transgenic mouse model for prostate cancer.

Results: Activation of p38MAPK was significantly elevated (2.

Enforced expression of FGF-7 promotes epithelial hyperplasia whereas a dominant negative FGFR2iiib promotes the emergence of neuroendocrine phenotype in prostate glands of transgenic mice.

The minimal rat probasin (PB) promoter was used to target expression of human fibroblast growth factor-7 (FGF-7)/keratinocyte growth factor (KGF) directly to prostatic epithelium of transgenic mice, converting FGF-7 from a paracrine to an autocrine factor. Four independent lines were established that expressed the transgene (PKS) in the prostate. Upon histologic analysis, the prostatic epithelium of PKS mice was found to be hyperplastic.