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Titolo:
In vitro studies of a prolactin antagonist, hPRL-G129R in human breast cancer cells
Autore:
Ramamoorthy, P; Sticca, R; Wagner, TE; Chen, WY;
Indirizzi:
Greenville Hosp Syst, Oncol Res Inst, Ctr Canc, Greenville, SC 29605 USA Greenville Hosp Syst Greenville SC USA 29605 nc, Greenville, SC 29605 USA Clemson Univ, Dept Microbiol & Mol Med, Clemson, SC 29681 USA Clemson Univ Clemson SC USA 29681 robiol & Mol Med, Clemson, SC 29681 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF ONCOLOGY
fascicolo: 1, volume: 18, anno: 2001,
pagine: 25 - 32
SICI:
1019-6439(200101)18:1<25:IVSOAP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPIDERMAL GROWTH-FACTOR; DNA FRAGMENTATION; RECEPTOR; EXPRESSION; INDUCTION; APOPTOSIS; PROLIFERATION; TGF-BETA-1; TAMOXIFEN; SECRETION;
Keywords:
prolactin antagonist; breast cancer; apoptosis; caspase-3; transforming growth factors; cisplatin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Chen, WY Greenville Hosp Syst, Oncol Res Inst, Ctr Canc, 700 W Faris Rd, Greenville, SC 29605 USA Greenville Hosp Syst 700 W Faris Rd Greenville SC USA 29605 5 USA
Citazione:
P. Ramamoorthy et al., "In vitro studies of a prolactin antagonist, hPRL-G129R in human breast cancer cells", INT J ONCOL, 18(1), 2001, pp. 25-32

Abstract

Human prolactin (hPRL) has been shown to be one of the important survival/growth factors that promotes the proliferation of breast cancer cells in anautocrine/paracrine manner. In our recent studies, we demonstrated that a hPRL antagonist with a single amino acid substitution mutation (hPRL-G129R)was able to inhibit breast cancer cell proliferation via induction of apoptosis (1). In this study three independent yet related experiments were carried out regarding the effects of hPRL-G129R in breast cancer cells. We investigated the possible mechanism(s) of hPRL-G129R induced apoptosis in breast cancer cells. It is well documented that transforming growth factors (TGF) in conjunction with hormones such as estrogen and PRL play a major role in modulating the proliferation and apoptosis of mammary cells. We first investigated the relationships between hPRL/hPRL-G129R and TGFs. We show thathPRL is able to down-regulate TGF beta1 (apoptotic factor) secretion and upregulate TGF alpha (survival factor) secretion in a dose-dependent manner in T-47D cells. More importantly the hPRL antagonist up-regulates TGF beta1and down-regulates TGF alpha secretion. When hPRL-G129R was applied together with hPRL, it blocked the effects of hPRL. Secondly, we tested the possible involvement of caspases in hPRL-G129R induced apoptosis. We have shown that caspase-3 is activated by hPRL-G129R at a concentration of 250 ng/ml in T-47D breast cancer cells. Thirdly, we explored the additive effects of an antineoplastic drug, cisplatin, with the hPRL-G129R in T47D breast cancercells. We show that cisplatin and hPRL-G129R when applied together resulted in about 40% growth inhibition in T-47D cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 18:08:06