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Titolo:
Altered growth regulation and loss of response to retinoic acid accompany tumorigenic transformation of prostatic cells
Autore:
Peehl, DM; Sellers, RG; Arnstein, P; Kung, HF; Rhim, JS;
Indirizzi:
Stanford Univ, Med Ctr, Dept Urol, Sch Med, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 Urol, Sch Med, Stanford, CA 94305 USA State Calif, Dept Hlth Serv, Viral & Rickettsial Dis Lab, Berkeley, CA 94704 USA State Calif Berkeley CA USA 94704 ettsial Dis Lab, Berkeley, CA 94704 USA Uniformed Serv Univ Hlth Sci, Ctr Prostate Dis Res, Rockville, MD 20852 USA Uniformed Serv Univ Hlth Sci Rockville MD USA 20852 ckville, MD 20852 USA
Titolo Testata:
ANTICANCER RESEARCH
fascicolo: 5B, volume: 19, anno: 1999,
pagine: 3857 - 3864
SICI:
0250-7005(199909/10)19:5B<3857:AGRALO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
V-KI-RAS; PAPILLOMAVIRUS TYPE-18 DNA; SIMIAN-VIRUS-40 T-ANTIGEN; EPITHELIAL-CELLS; FACTOR RECEPTOR; NEOPLASTIC TRANSFORMATION; CANCER PROGRESSION; PRIMARY CULTURES; TRANSGENIC MICE; GENE-EXPRESSION;
Keywords:
prostate cancer; human papillomavirus; retinoic acid; epidermal growth factor; vitamin D; insulin-like growth factor; transforming growth factor-beta;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Peehl, DM Stanford Univ, Med Ctr, Dept Urol, Sch Med, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 Med, Stanford, CA 94305 USA
Citazione:
D.M. Peehl et al., "Altered growth regulation and loss of response to retinoic acid accompany tumorigenic transformation of prostatic cells", ANTICANC R, 19(5B), 1999, pp. 3857-3864

Abstract

In vitro models of human prostatic carcinogenesis are increasingly available and include representatives of normal, immortal, tumorigenic and metastatic phenotypes. In this study, growth regulation of immortal, but non-tumorigenic, human papillomavirus-transformed prostatic epithelial cells was compared to that of their tumorigenic variants. These variants were created either by exposure to a carcinogen or by passage through mice. In all cases, tumorigenic cells retained responsiveness to a potent mitogen, epidermal growth factor, and to a potent growth inhibitory factor; 1,25-dihydroxyvitamin D-3. Responses to other growth regulatory factors were altered One set oftransformants, CA-HPV-10 and its tumorigenic variants 5019 and 5019IIc, lost their requirement for insulin-like growth factor. Another set, RWPE-1 and its tumorigenic variant 129Nu5002-1 Tu, became unresponsive to growth inhibition by transforming growth factor-beta. The only alteration uniquely con elated with the tumorigenic phenotype was loss of response to retinoic acid. This factor; which inhibits growth of normal and immortal but non-tumorigenic prostatic epithelial cells, had no effect on tumorigenic 129Nu5002-1Tu cells. We previously reported that conversion of an SV40-immortalized prostatic epithelial cell line to tumorigenicity by introduction of the ras oncogene also resulted in loss of responsiveness to growth inhibitory activity of retinoic acid. 129Nu5002-1 Tu cells, which do not have an altered ras gene, gained the same phenotype. This suggests that loss of inhibition byretinoic acid may be a critical element in the tumorigenic conversion of prostatic epithelial cells.

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Documento generato il 23/01/20 alle ore 06:32:05