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Titolo:
RADIATION INACTIVATION OF HUMAN PROSTATE-CANCER CELLS - THE ROLE OF APOPTOSIS
Autore:
ALGAN O; STOBBE CC; HELT AM; HANKS GE; CHAPMAN JD;
Indirizzi:
FOX CHASE CANC CTR,DEPT RADIAT ONCOL,7701 BURHOLME AVE PHILADELPHIA PA 19111
Titolo Testata:
Radiation research
fascicolo: 3, volume: 146, anno: 1996,
pagine: 267 - 275
SICI:
0033-7587(1996)146:3<267:RIOHPC>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA FRAGMENTATION; GAMMA-IRRADIATION; BETA-LAPACHONE; ENDONUCLEASE; BCL-2; ACTIVATION; CALCIUM; DEATH; EXPRESSION; INDUCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
O. Algan et al., "RADIATION INACTIVATION OF HUMAN PROSTATE-CANCER CELLS - THE ROLE OF APOPTOSIS", Radiation research, 146(3), 1996, pp. 267-275

Abstract

Radiation-induced apoptosis detected by gel electrophoresis was measured in cells of three human prostate carcinoma cell lines (TSU, PC-3 and DU-145) and compared to their intrinsic radiosensitivities as measured by clonogenic assays. The intrinsic radiosensitivities of each cell line were defined by their alpha and beta coefficients and their surviving fraction at 2 Gy, derived from complete survival curves. The temporal expression and kinetics of radiation-induced apoptosis for DU-145 cells, the human prostate carcinoma cell line which expressed the highest rate of radiation-induced apoptosis, was characterized further by differential sedimentation and the immunofluorescence assay (Apoptag(R)) which was specific for 3'-OH ends in cellular DNA. Cell viability was measured microscopically with trypan blue staining. Cell survival after various doses was computer-fitted to either a simple linear ora linear-quadratic equation. Twenty-four hours after a 10-Gy dose of Cs-137 gamma rays, DNA fragmentation to nucleosome multimers was strongly expressed in only DU-145 cells. In this cell line, when centrifugation at 12,000 g for 10 min was used to separate fragmented from largemolecular weight DNA, the proportion of DNA in the supernatant increased to a maximum of similar to 17% of the total by 10-12 h after radiation treatment. Cell death 24 h after irradiation measured by trypan blue exclusion assays followed single-hit kinetics up to 80 Gy. The proportion of cells which were labeled with Apoptag(R) displayed single-hit kinetics and yielded the same inactivation coefficient as measured by trypan blue. Together, these data indicate that the rapid (24 h) inactivation of irradiated DU-145 cells results from apoptosis and accounts for about 5% of the single-hit killing measured by clonogenic assay. Temporal studies of radiation-induced killing of DU-145 cells distinguished this rapid mechanism of cell death from the major mechanism (72-144 h). These may correlate with apoptosis and proliferative cell death, respectively. Of the three prostate cancer cell lines investigated, only DU-145 cells displayed significant levels of radiation-induced DNA fragmentation and rapid cell death, with characteristics of apoptosis. This mechanism of cell death was complete by 24 h after irradiation and was well separated in time from the death of cells by the major mechanism(s) which occurred after 72 h, and accounted for about 5% of cell inactivation by a single-hit mechanism. (C) 1996 by Radiation Research Society

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 14:04:28