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Titolo:
X-irradiation enhances the expression of Bcl-2 in HL-60 cells: The resulting effects on apoptosis and radiosensitivity
Autore:
Kariya, S; Ogawa, Y; Yoshida, S; Yabuki, M; Imajo, Y; Utsumi, K;
Indirizzi:
Kochi Med Sch, Dept Radiol, Nankoku, Kochi 7835805, Japan Kochi Med Sch Nankoku Kochi Japan 7835805 , Nankoku, Kochi 7835805, Japan Kurashiki Med Ctr, Inst Med Sci, Kurashiki, Okayama, Japan Kurashiki Med Ctr Kurashiki Okayama Japan Sci, Kurashiki, Okayama, Japan Kawasaki Med Sch, Dept Radiol, Kurashiki, Okayama, Japan Kawasaki Med SchKurashiki Okayama Japan diol, Kurashiki, Okayama, Japan
Titolo Testata:
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
fascicolo: 2, volume: 3, anno: 1999,
pagine: 145 - 152
SICI:
1107-3756(199902)3:2<145:XETEOB>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOGENOUS ENDONUCLEASE ACTIVATION; ICE/CED-3 PROTEASE; CYCLE CHECKPOINT; CANCER-CELLS; C-MYC; DEATH; P53; OXYGEN; ALPHA; GENE;
Keywords:
radiation; apoptosis; HL-60 cell; Bcl-2; cell cycle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Kariya, S Kochi Med Sch, Dept Radiol, Oko Cho, Nankoku, Kochi 7835805, Japan Kochi Med Sch Oko Cho Nankoku Kochi Japan 7835805 7835805, Japan
Citazione:
S. Kariya et al., "X-irradiation enhances the expression of Bcl-2 in HL-60 cells: The resulting effects on apoptosis and radiosensitivity", INT J MOL M, 3(2), 1999, pp. 145-152

Abstract

Although p53 has been shown to directly activate transcriptional bax gene and to inhibit expression of bcl-2 gene during radiation-induced apoptosis,it is poorly understood how the Bcl-2 family changes, in p53-deficient cells: during radiation-induced apoptosis. The present work describes the effect of X-irradiation on the apoptosis of p53-deficient HL-60 cells as assessed by means of several methods. Apoptosis of HL-60 cells was induced by X-irradiation in a dose- and time-dependent manner. 18 h after 5 Gy irradiation, G(2) cells underwent apoptosis, while 15 Gy X-irradiation induced the death of G(1)/S cells by 6 h. After X-irradiation, expression of Bcl-2 was elevated, while Bar expression was unchanged. We have isolated a clonal HL-60variant following twice 5 Gy irradiation of HL-XR3 cells. These cells highly expressed Bcl-2 (about 2-fold), showed a reduced activation of caspase-3, and were not only more resistant to X-irradiation-induced apoptosis but also more radioresistant. These results suggest that HL-60 cells may resist apoptosis and radiation by increasing Bcl-2 expression, and that this elevated Bcl-2 expression might be one of the causes of the phenomenon, often seen clinically, that tumor cells gradually acquire radioresistance during fractionated radiation therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 05:15:09