Transforming growth factor-β in benign and malignant prostate

Chung Lee*, Sharon M. Sintich, Eric P. Mathews, Ali H. Shah, Shilajit D Kundu, Kent T Perry Jr, Jin Seon Cho, Kenneth Y. Ilio, Marcus V. Cronauer, Lynn Janulis, Julia A. Sensibar

*Corresponding author for this work

Research output: Contribution to journalArticle

132 Citations (Scopus)

Abstract

BACKGROUND. The present review summarizes the cellular action of TGF-β in benign and malignant growth of the prostate. METHODS. TGF-β 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- β 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-β action. These include the loss of expression of functional TGF-β receptors and overproduction of TGF-β in malignant cells. The loss of expression of functional TGF-β receptors provides a growth advantage to cancer cells over their benign counterparts. The overproduction of TGF-β by cancer cells has a multitude of adverse consequences. TGF-β 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-β seems to be the primary cause of tumor progression. This is because, if these cancer cells were engineered to reduce the production of TGF-β, 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.

Original languageEnglish (US)
Pages (from-to)285-290
Number of pages6
JournalProstate
Volume39
Issue number4
DOIs
StatePublished - Jun 1 1999

Fingerprint

Transforming Growth Factors
Prostate
Prostatic Neoplasms
Neoplasms
Growth
Smooth Muscle
Epithelium
Prostatic Hyperplasia
Immunosuppressive Agents
Extracellular Matrix
Intercellular Signaling Peptides and Proteins
Homeostasis
Epithelial Cells
Apoptosis

ASJC Scopus subject areas

  • Oncology
  • Urology

Cite this

Lee, Chung ; Sintich, Sharon M. ; Mathews, Eric P. ; Shah, Ali H. ; Kundu, Shilajit D ; Perry Jr, Kent T ; Cho, Jin Seon ; Ilio, Kenneth Y. ; Cronauer, Marcus V. ; Janulis, Lynn ; Sensibar, Julia A. / Transforming growth factor-β in benign and malignant prostate. In: Prostate. 1999 ; Vol. 39, No. 4. pp. 285-290.
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abstract = "BACKGROUND. The present review summarizes the cellular action of TGF-β in benign and malignant growth of the prostate. METHODS. TGF-β 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- β 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-β action. These include the loss of expression of functional TGF-β receptors and overproduction of TGF-β in malignant cells. The loss of expression of functional TGF-β receptors provides a growth advantage to cancer cells over their benign counterparts. The overproduction of TGF-β by cancer cells has a multitude of adverse consequences. TGF-β 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-β seems to be the primary cause of tumor progression. This is because, if these cancer cells were engineered to reduce the production of TGF-β, 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.",
author = "Chung Lee and Sintich, {Sharon M.} and Mathews, {Eric P.} and Shah, {Ali H.} and Kundu, {Shilajit D} and {Perry Jr}, {Kent T} and Cho, {Jin Seon} and Ilio, {Kenneth Y.} and Cronauer, {Marcus V.} and Lynn Janulis and Sensibar, {Julia A.}",
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Lee, C, Sintich, SM, Mathews, EP, Shah, AH, Kundu, SD, Perry Jr, KT, Cho, JS, Ilio, KY, Cronauer, MV, Janulis, L & Sensibar, JA 1999, 'Transforming growth factor-β in benign and malignant prostate', Prostate, vol. 39, no. 4, pp. 285-290. https://doi.org/10.1002/(SICI)1097-0045(19990601)39:4<285::AID-PROS9>3.0.CO;2-7

Transforming growth factor-β in benign and malignant prostate. / Lee, Chung; Sintich, Sharon M.; Mathews, Eric P.; Shah, Ali H.; Kundu, Shilajit D; Perry Jr, Kent T; Cho, Jin Seon; Ilio, Kenneth Y.; Cronauer, Marcus V.; Janulis, Lynn; Sensibar, Julia A.

In: Prostate, Vol. 39, No. 4, 01.06.1999, p. 285-290.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Transforming growth factor-β in benign and malignant prostate

AU - Lee, Chung

AU - Sintich, Sharon M.

AU - Mathews, Eric P.

AU - Shah, Ali H.

AU - Kundu, Shilajit D

AU - Perry Jr, Kent T

AU - Cho, Jin Seon

AU - Ilio, Kenneth Y.

AU - Cronauer, Marcus V.

AU - Janulis, Lynn

AU - Sensibar, Julia A.

PY - 1999/6/1

Y1 - 1999/6/1

N2 - BACKGROUND. The present review summarizes the cellular action of TGF-β in benign and malignant growth of the prostate. METHODS. TGF-β 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- β 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-β action. These include the loss of expression of functional TGF-β receptors and overproduction of TGF-β in malignant cells. The loss of expression of functional TGF-β receptors provides a growth advantage to cancer cells over their benign counterparts. The overproduction of TGF-β by cancer cells has a multitude of adverse consequences. TGF-β 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-β seems to be the primary cause of tumor progression. This is because, if these cancer cells were engineered to reduce the production of TGF-β, 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.

AB - BACKGROUND. The present review summarizes the cellular action of TGF-β in benign and malignant growth of the prostate. METHODS. TGF-β 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- β 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-β action. These include the loss of expression of functional TGF-β receptors and overproduction of TGF-β in malignant cells. The loss of expression of functional TGF-β receptors provides a growth advantage to cancer cells over their benign counterparts. The overproduction of TGF-β by cancer cells has a multitude of adverse consequences. TGF-β 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-β seems to be the primary cause of tumor progression. This is because, if these cancer cells were engineered to reduce the production of TGF-β, 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.

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