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Constitutive expression of FGF2/bFGF in non‐tumorigenic human prostatic epithelial cells results in the acquisition of a partial neoplastic phenotype
Author(s) -
Ropiquet Frédéric,
Berthon Philippe,
Villette JeanMarie,
Le Brun Gaëlle,
Maitland Norman J.,
Cussenot Olivier,
Fiet Jean
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970729)72:3<543::aid-ijc26>3.0.co;2-b
Subject(s) - phenotype , cancer research , biology , pathology , gene , medicine , genetics
Fibroblast growth factor 2 (FGF2), also known as basic fibroblast growth factor (bFGF), belongs to the FGF family, which consists of at least 9 closely related members. FGF2 is a potent mitogen for fibroblasts derived from normal prostate and, to a lesser extent, for prostatic epithelial cells. Its role in the physiology of the normal prostate seems to be limited to stromal cells, whereas in prostate cancer FGF2 may also have an autocrine/paracrine effect on epithelial cells. In order to better understand the effects of FGF2 on the prostatic epithelium, especially its role in the progression of prostate cancer by establishing an autocrine‐stimulation loop, we transfected FGF2 cDNA into a human prostatic epithelial cell line, PNT1A, immortalized with SV40 large‐T antigen. This cell line is non‐tumorigenic and expresses a high‐affinity FGF2 receptor, FGFR1/flg. We characterized 3 independent FGF2‐transfected clones and found that the establishment of an FGF2 autocrine loop on these cells led to (i) serum‐independent growth, (ii) increased proliferation and (iii) anchorage‐independent growth. Such results argue in favor of the possible action of FGF2 on progression of prostate cancer via an FGF2 autocrine loop on epithelial cells. Int. J. Cancer 72:543–547, 1997. © 1997 Wiley‐Liss, Inc.