Roles of cAMP and cAMP-dependent protein kinase in the progression of prostate cancer: cross-talk with the androgen receptor.
Prostate carcinomas are among the most frequently diagnosed and death causing cancers affecting males in the developed world. It has become clear that the molecular mechanisms that drive the differentiation of normal prostate cells towards neoplasia involve multiple signal transduction cascades that often overlap and interact. A critical mediator of cellular proliferation and differentiation in various cells (and cancers) is the cAMP-dependent protein kinase, also known as protein kinase A (PKA), and its activating secondary messenger, cAMP. PKA and cAMP have been shown to play critical roles in prostate carcinogenesis and are the subject of this review. In particular we will focus on the cross-talk between PKA/cAMP signaling and that of the androgen receptor.
Merkle
Dennis
D
Philips Research, High Tech Campus, 5656AE, Eindhoven,The Netherlands. dennis.merkle@philips.com
Hoffmann
Ralf
R
D000728:Androgens / Q000378:metabolism; D002454:Cell Differentiation; D000242:Cyclic AMP / Q000378:metabolism*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000502:physiology*; D006801:Humans; D008297:Male; D055099:Neuroendocrine Cells / Q000473:pathology; D011471:Prostatic Neoplasms / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology*; D011944:Receptors, Androgen / Q000096:biosynthesis / Q000502:physiology*; D015398:Signal Transduction
D000728:Androgens; D011944:Receptors, Androgen; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases