Premium
Radiation‐induced apoptosis in human ovarian carcinoma cells growing as a monolayer and as multicell spheroids
Author(s) -
Filippovich Igor V.,
Sorokitalya I.,
Robillard Nelly,
Chatal JeanFrançois
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970904)72:5<851::aid-ijc23>3.0.co;2-a
Subject(s) - apoptosis , trypan blue , necrosis , acridine orange , spheroid , biology , cell cycle , programmed cell death , cell culture , cell , microbiology and biotechnology , andrology , medicine , biochemistry , genetics
Response to external gamma irradiation was studied in a human ovarian carcinoma cell line (OVCAR 3) growing as a monolayer and as multicell spheroids. Necrosis and apoptosis were documented using Trypan‐blue uptake and acridine‐orange staining, respectively, and apoptosis was quantified using a terminal deoxynucleotidyl transferase assay. Exposure of OVCAR 3 cells growing as a monolayer to 137 Cs gamma radiation at a dose of 10 Gy produced 30–40% apoptosis 72 hr after irradiation. Cell‐cycle analysis of irradiated cells showed an accumulation of cells in G 2 /M phase 24 hr after irradiation and then a decline at 48 hr in conjunction with apoptosis onset. The loss of G 0 /G 1 cells in irradiated cultures suggested a preferential entry into apoptosis. No increase in apoptotic cell number was observed in OVCAR 3 spheroids after irradiation, and the cells probably died as a result of necrosis. When spheroids were disrupted immediately after irradiation to obtain a cell suspension, minor apoptosis was observed in association with a marked increase in TB‐positive cell number after 96 hr of incubation following irradiation. Thus, a relationship was found between radiation‐induced apoptosis and the cell cycle. Results with spheroids suggested the possible involvement of cell‐to‐cell interactions in apoptosis regulation. Int. J. Cancer 72:851–859, 1997. © 1997 Wiley‐Liss, Inc.