Potential Role of HBGF (FGF) and TGF-Beta on Prostate Growth

Matuo, Yuhsi; McKeehan, Wallace L.; Yan, Guochen; Nikolaropoulos, Stathis; Adams, Pamela S.; Fukabori, Yoshitatsu; Yamanaka, Hidetoshi; Gaudreau, Josette

doi:10.1007/978-1-4615-3398-6_11

Cited by 22 publications

(7 citation statements)

References 11 publications

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“…The exon IIIbcontaining receptor isoform is an epithelial-specific isoform which has a high affinity for stromal cellderived FGF7 (KGF), whereas the isoform containing exon IIIc recognizes and responds to bFGF. Inhibition of bFGF translation by application of antisense oligonucleotides was shown to slow down growth of the AT-3 Dunning tumor, which is also in line with autocrine bFGF growth stimulation [106].…”

Section: Fibroblast Growth Factors In the Prostate: Keys To Cell Intementioning

confidence: 68%

Regulation of prostatic growth and function by peptide growth factors

et al. 1996

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Polypeptide growth factors are positive and negative regulators of prostatic growth and function. Expression and biological effects of epidermal growth factor (EGF), transforming growth factors (TGFs) α and β, fibroblast growth factors (FGFs), and insulin‐like growth factors (IGFs) in the prostate have been extensively studied. EGF and TGFα, which share the same receptor, are strong mitogens for prostatic epithelial and stromal cells. Their paracrine mode of action in normal tissue and early‐stage tumors is apparently altered towards an autocrine stimulation in hormone‐independent tumors, which gain the ability to produce TGFα by themselves. TGFβ has a dual role in the regulation of prostatic growth. It inhibits growth of prostatic epithelial cells in culture and mediates programmed cell death after androgen withdrawal. However, advanced prostatic carcinomas become insensitive to the inhibitory effect of TGFβ. Several members of the FGF family have been identified in the prostate. They are mainly or exclusively expressed in the stromal cells, and stimulate the epithelial cells. In the rat Dunning tumor model, progression is accompanied by distinct changes in the expression of FGFs and their receptors. In the hyperplastic tissue, basic FGF (bFGF) is accumulated. This growth factor is also a potent angiogenic inducer, expression of which may determine the metastatic capability of a tumor. IGFs are paracrine growth stimulators in the normal and hyperplastic prostate. It is still under consideration whether prostatic cancer cells gain the ability to produce IGF‐I by themselves and thus shift to an autocrine mode of IGF‐I stimulation. Growth factors also interact with the androgen‐signaling pathway. IGF‐I in particular, other growth factors as well, can activate the androgen receptor. © 1996 Wiley‐Liss, Inc.

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Section: Fibroblast Growth Factors In the Prostate: Keys To Cell Intementioning

confidence: 68%

Regulation of prostatic growth and function by peptide growth factors

et al. 1996

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“…TGFb1 may also facilitate detachment and metastasis. 76 An additional important mechanism of tumor growth promotion by TGFb1 may be via autocrine stimulation of endothelin-1, implicated in prostate tumor progression. 77 Thus, it may be speculated that in the absence of PTEN and/or p53, Egr1 becomes an oncogenic agent in prostate cancer via the effects of its target genes, fibronectin and TGFb1.…”

Section: Egr1-induced Oncogenesis Of Prostate Cancermentioning

confidence: 99%

The transcription factor Egr1 is a direct regulator of multiple tumor suppressors including TGFβ1, PTEN, p53, and fibronectin

Bar-On

Adamson

Calogero³

et al. 2005

Cancer Gene Ther

325

281

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Recent studies are reviewed indicating that the transcription factor early growth response-1 (Egr1) is a direct regulator of multiple tumor suppressors including TGFb1, PTEN, p53, and fibronectin. The downstream pathways of these factors display multiple nodes of interaction with each other, suggesting the existence of a functional network of suppressor factors that serve to maintain normal growth regulation and resist the emergence of transformed variants. Paradoxically, Egr1 is oncogenic in prostate cancer. In the majority of these cancers, PTEN or p53 is inactive. It is suggested that these defects in the suppressor network allow for the unopposed induction of TGFb1 and fibronectin, which favor transformation and survival of prostate tumor epithelial cells, and explain the role of Egr1 in prostate cancer. Egr1 is a novel and logical target for intervention by gene therapy methods, and targeting methods are discussed.

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“…The mesenchyme probably influences normal epithelial function by two different, but interacting, receptormediated systems: growth factors derived from the stromal compartment and components of the extracellular matrix. There is considerable evidence indicating that the growth and proliferation of epithelial cells in the prostate is influenced by factors such as EGF, TGF-a, TGF-P, nerve growth factor (NGF) and members of the IGF and FGF families (Mori et al 1990;Thompson 1990;Djakiew et al 1991;Gleave et al 1991;Cohen et al 1991;Hofer et al 1991;Wilding 1991;Story 1991;Matuo et al 1992;Chung et al 1992). Recent evidence has suggested that the interaction of some of these growth factors with their cognate receptors, in particular FGF-7, requires both the specific epithelial receptor and defined components of the extracellular matrix, particularly heparan sulfate (McKeehan et al 1984;McKeehan 1991;Yan et al 1992;Kan et al 1993).…”

Section: Role Of the Extracellular Matrix Proteases And Growthmentioning

confidence: 99%

The role of growth factors in the suppression of active cell death in the prostate: an hypothesis

Guenette¹,

Tenniswood²

1994

Biochem. Cell Biol.

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Regression of the rat ventral prostate occurs when the level of 5 alpha-dihydrotestosterone, the trophic hormone, drops below the threshold required to suppress apoptosis. The induction of apoptosis in the ventral prostate is accompanied by the increase in the steady-state level of a number of mRNAs coding for proteins that are involved in the latter stages of apoptosis and thus represent secondary thanatogens. These include proteases (cathepsins, plasminogen activators, and collagenase), clusterin, poly(ADP)ribose polymerase, tenascin, and several unidentified genes, as well as several RNases and the classical Ca2+,Mg(2+)-dependent endonuclease. In addition, insulin-like growth-factor-binding protein 5 (IGFBP-5) is induced de novo. We propose that IGFBP-5 may serve to trigger the apoptotic process through the attenuation of the insulin-like growth factor signalling system (which is necessary for cell survival), and as such, represents a primary thanatogen in the prostate.

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Potential Role of HBGF (FGF) and TGF-Beta on Prostate Growth

Cited by 22 publications

References 11 publications

Regulation of prostatic growth and function by peptide growth factors

Regulation of prostatic growth and function by peptide growth factors

The transcription factor Egr1 is a direct regulator of multiple tumor suppressors including TGFβ1, PTEN, p53, and fibronectin

The role of growth factors in the suppression of active cell death in the prostate: an hypothesis

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