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Titolo:
In vivo veritas: Bcl-2 and Bcl-X-L mediate tumor cell resistance to chemotherapy
Autore:
Fujita, N; Tsuruo, T;
Indirizzi:
Univ Tokyo, Inst Mol & Cellular Biosci, Dept Biomed Res, Bunkyo Ku, Tokyo 1130032, Japan Univ Tokyo Tokyo Japan 1130032 omed Res, Bunkyo Ku, Tokyo 1130032, Japan
Titolo Testata:
DRUG RESISTANCE UPDATES
fascicolo: 3, volume: 3, anno: 2000,
pagine: 149 - 154
SICI:
1368-7646(2000)3:3<149:IVVBAB>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
T-LYMPHOMA CELLS; MULTIDRUG-RESISTANCE; INDUCED APOPTOSIS; CLONOGENIC SURVIVAL; CANCER-CELLS; DEATH; BAX; EXPRESSION; PROTEIN; BCL-X(L);
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Tsuruo, T Univ Tokyo, Inst Mol & Cellular Biosci, Dept Biomed Res, Bunkyo Ku, 1-1-1 Yayoi, Tokyo 1130032, Japan Univ Tokyo 1-1-1 Yayoi Tokyo Japan 1130032 Tokyo 1130032, Japan
Citazione:
N. Fujita e T. Tsuruo, "In vivo veritas: Bcl-2 and Bcl-X-L mediate tumor cell resistance to chemotherapy", DRUG RESIST, 3(3), 2000, pp. 149-154

Abstract

Apoptosis is cellular suicide, the functional opposite of mitosis. It may play an important role in tissue growth control and removal of damaged and premalignant cells. The fact that diverse chemotherapeutic agents induce apoptosis, while they engage different intracellular targets and cause DNA damage, raises a concern that tumors resistant to chemotherapy are unable to initiate the apoptotic process. The anti-apoptotic Bcl-2 family proteins, Bcl-2 and Bcl-X-L, play an important role in the regulation of apoptotic cell death. Bcl-2 and Bcl-X-L have been reported to confer chemotherapy resistance in short-term survival assays in vitro. However, they failed to provide a long-term clonogenic survival advantage. Thus, the role of anti-apoptotic Bcl-2 and Bcl-X-L on chemotherapy resistance in vivo remains unclear. Invivo, tumor cells receive survival signals from the extracellular microenvironment. Since the microenvironmental factors have been reported to modulate the expression and function of Bcl-2 family proteins, Bcl-2 and Bcl-X-L might be associated with the chemotherapy resistance in vivo through the influence of these factors. Consistent with this hypothesis, several investigators have recently reported that the sensitivity to chemotherapy in in vitro clonogenic assays did not correlate with that in in vivo tumor models. The lack of microenvironmental factors might cause the discrepancy between in vitro clonogenic growth and in vivo tumor growth. These results suggest that Bcl-2 and Bcl-X-L could contribute to chemotherapy resistance in vivo, along with already defined drug resistance mechanisms (i.e. P-glycoprotein,MRP). Therapies aimed at suppressing the expression and function of Bcl-2 and Bcl-X-L or at intercepting microenvironmental factors might successfully overcome chemotherapy resistance. (C) 2000 Harcourt Publishers Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 16:00:51