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Efectos del tratamiento prolongado con AZT sobre células tumorales: acortamiento telomérico, inducción de senescencia y apoptosis, y reducción de tumorigenicidad
Agueda Mercedes Tejera Daniel E. Gomez
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Resumen/Descripción – provisto por el repositorio digital
Normal cells in culture divide a certain amount of times and undergo a process termed replicative senescence. Telomere loss is thought to control entry into senescence. Activation of telomerase in tumors bypasses cellular senescence and is thus a requirement for tumor progression. In this work, we have investigated the effects of chronic in vitro 3'-azido-2', 3'-dideoxythymidine (AZT)exposure on human and murine carcinoma cells. We demonstrate the irreversible telomere shortening in human cervical cancer cells (HeLa) cultured for long-term with AZT, but without evidence of senescence. Furthermore, we demonstrate, for the first time, that AZT-treated murine mammary carcinoma cells (F3II) have a reduced tumorigenicity in syngeneic BALB/c mice. Tumor incidence was reduced and survival was prolonged in animals inoculated with AZT-treated cells when comparing with control counterparts. The number and size of spontaneous metastases were also decreased in animals receiving AZT-treated F3II cells. In addition, we present morphological and biochemical evidence of senescence, and induction of apoptosis in tumor cells exposed to AZT. These data indicate that chronic exposure of mammary carcinoma cells to AZT may be sufficient to induce a senescent phenotype and to reduce tumorigenicity.Palabras clave – provistas por el repositorio digital
APOPTOSIS; AZT; CANCER DE MAMA; SENESCENCIA; TELOMERASA; BREAST CANCER; SENESCENCE; TELOMERASE
Disponibilidad
| Institución detectada | Año de publicación | Navegá | Descargá | Solicitá |
|---|---|---|---|---|
| No requiere | 2002 | Biblioteca Digital (FCEN-UBA) (SNRD) |
|
Información
Tipo de recurso:
tesis
Idiomas de la publicación
- español castellano
País de edición
Argentina
Fecha de publicación
2002
Información sobre licencias CC