title: Transforming growth factor-beta in benign and malignant prostate.
abstract: BACKGROUND
  The present review summarizes the cellular action of TGF-beta in benign and malignant growth of the prostate.
  
  
  METHODS
  TGF-beta is a pleiotropic growth factor. It plays an important role in the regulation of growth and differentiation in many cells. In benign prostatic epithelia, its action is mediated through a paracrine mechanism. It inhibits proliferation and induces apoptosis in prostatic epithelia. It provides a mechanism to maintain epithelial homeostasis in the prostate. In prostatic stroma, its continual action leads to smooth muscle differentiation. This effect of TGF-beta may regulate the development of prostatic smooth muscle nodules in benign prostatic hyperplasia.
  
  
  RESULTS
  As prostatic epithelial cells undergo malignant transformation, two major events occur regarding TGF-beta action. These include the loss of expression of functional TGF-beta receptors and overproduction of TGF-beta in malignant cells. The loss of expression of functional TGF-beta receptors provides a growth advantage to cancer cells over their benign counterparts. The overproduction of TGF-beta by cancer cells has a multitude of adverse consequences. TGF-beta can promote extracellular matrix production, induce angiogenesis, and inhibit host immune function. The biological consequence of these activities is an enhanced tumorigenicity in prostate cancer. Results of our recent studies with a rat prostate cancer model suggest that the immunosuppressive effect of TGF-beta seems to be the primary cause of tumor progression. This is because, if these cancer cells were engineered to reduce the production of TGF-beta, tumor growth was inhibited in syngeneic hosts but not in immune compromised hosts.
  
  
  CONCLUSIONS
  Our future research should take advantage of this knowledge to devise therapeutic strategies aimed at eradicating prostate cancer.
authors.affiliation: Department of Urology, Northwestern University Medical School, Chicago, Illinois 60611, USA. c-lee7@nwu.edu
authors.forename: C
authors.initials: C
authors.lastname: Lee
authors.forename: S M
authors.initials: SM
authors.lastname: Sintich
authors.forename: E P
authors.initials: EP
authors.lastname: Mathews
authors.forename: A H
authors.initials: AH
authors.lastname: Shah
authors.forename: S D
authors.initials: SD
authors.lastname: Kundu
authors.forename: K T
authors.initials: KT
authors.lastname: Perry
authors.forename: J S
authors.initials: JS
authors.lastname: Cho
authors.forename: K Y
authors.initials: KY
authors.lastname: Ilio
authors.forename: M V
authors.initials: MV
authors.lastname: Cronauer
authors.forename: L
authors.initials: L
authors.lastname: Janulis
authors.forename: J A
authors.initials: JA
authors.lastname: Sensibar
mesh_terms: D000728:Androgens / Q000378:metabolism; D000818:Animals; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D011379:Prognosis; D011470:Prostatic Hyperplasia / Q000378:metabolism* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000473:pathology; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D000728:Androgens; D016212:Transforming Growth Factor beta