Cisplatin induces apoptosis in a human ovarian carcinoma cell line without concomitant internucleosomal degradation of DNA

After treatment of the human ovarian carcinoma cell line, CH1, with cisplatin, cells detached from the culture dish in a time- and dose-dependent fashion. These cells showed morphological changes indicative of apoptosis. Their DNA had not been degraded into oligonucleosomal fragments, but the DNA ha...

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Published in:	Experimental cell research Vol. 211; no. 2; p. 231
Main Authors:	Ormerod, M G, O'Neill, C F, Robertson, D, Harrap, K R
Format:	Journal Article
Language:	English
Published:	United States 01.04.1994
Subjects:	Apoptosis - drug effects Apoptosis - physiology Cell Adhesion - drug effects Cisplatin - pharmacology DNA, Neoplasm - chemistry DNA, Neoplasm - metabolism Female Humans Microscopy, Electron Molecular Weight Nucleosomes - drug effects Nucleosomes - metabolism Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Tumor Cells, Cultured - drug effects Tumor Cells, Cultured - metabolism Tumor Cells, Cultured - pathology
ISSN:	0014-4827
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Abstract	After treatment of the human ovarian carcinoma cell line, CH1, with cisplatin, cells detached from the culture dish in a time- and dose-dependent fashion. These cells showed morphological changes indicative of apoptosis. Their DNA had not been degraded into oligonucleosomal fragments, but the DNA had been cut into larger fragments (30 kbp) of a size associated with chromatin loops. We conclude that cisplatin killed these ovarian cells by inducing apoptosis. However, in these cells, apoptosis was not accompanied by internucleosomal degradation of DNA. Our data are consistent with the hypothesis that the introduction of a double-strand break at a specific site in the chromatin loops is an early event in apoptosis. This degradation is accompanied by morphologically observable changes in chromatin structure. Internucleosomal degradation, when it occurs, is a late event.
AbstractList	After treatment of the human ovarian carcinoma cell line, CH1, with cisplatin, cells detached from the culture dish in a time- and dose-dependent fashion. These cells showed morphological changes indicative of apoptosis. Their DNA had not been degraded into oligonucleosomal fragments, but the DNA had been cut into larger fragments (30 kbp) of a size associated with chromatin loops. We conclude that cisplatin killed these ovarian cells by inducing apoptosis. However, in these cells, apoptosis was not accompanied by internucleosomal degradation of DNA. Our data are consistent with the hypothesis that the introduction of a double-strand break at a specific site in the chromatin loops is an early event in apoptosis. This degradation is accompanied by morphologically observable changes in chromatin structure. Internucleosomal degradation, when it occurs, is a late event. After treatment of the human ovarian carcinoma cell line, CH1, with cisplatin, cells detached from the culture dish in a time- and dose-dependent fashion. These cells showed morphological changes indicative of apoptosis. Their DNA had not been degraded into oligonucleosomal fragments, but the DNA had been cut into larger fragments (30 kbp) of a size associated with chromatin loops. We conclude that cisplatin killed these ovarian cells by inducing apoptosis. However, in these cells, apoptosis was not accompanied by internucleosomal degradation of DNA. Our data are consistent with the hypothesis that the introduction of a double-strand break at a specific site in the chromatin loops is an early event in apoptosis. This degradation is accompanied by morphologically observable changes in chromatin structure. Internucleosomal degradation, when it occurs, is a late event.After treatment of the human ovarian carcinoma cell line, CH1, with cisplatin, cells detached from the culture dish in a time- and dose-dependent fashion. These cells showed morphological changes indicative of apoptosis. Their DNA had not been degraded into oligonucleosomal fragments, but the DNA had been cut into larger fragments (30 kbp) of a size associated with chromatin loops. We conclude that cisplatin killed these ovarian cells by inducing apoptosis. However, in these cells, apoptosis was not accompanied by internucleosomal degradation of DNA. Our data are consistent with the hypothesis that the introduction of a double-strand break at a specific site in the chromatin loops is an early event in apoptosis. This degradation is accompanied by morphologically observable changes in chromatin structure. Internucleosomal degradation, when it occurs, is a late event.
Author	Robertson, D Ormerod, M G Harrap, K R O'Neill, C F
Author_xml	– sequence: 1 givenname: M G surname: Ormerod fullname: Ormerod, M G organization: Section of Drug Development, Institute of Cancer Research: Royal Cancer Hospital, Sutton, United Kingdom – sequence: 2 givenname: C F surname: O'Neill fullname: O'Neill, C F – sequence: 3 givenname: D surname: Robertson fullname: Robertson, D – sequence: 4 givenname: K R surname: Harrap fullname: Harrap, K R
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SubjectTerms	Apoptosis - drug effects Apoptosis - physiology Cell Adhesion - drug effects Cisplatin - pharmacology DNA, Neoplasm - chemistry DNA, Neoplasm - metabolism Female Humans Microscopy, Electron Molecular Weight Nucleosomes - drug effects Nucleosomes - metabolism Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Tumor Cells, Cultured - drug effects Tumor Cells, Cultured - metabolism Tumor Cells, Cultured - pathology
Title	Cisplatin induces apoptosis in a human ovarian carcinoma cell line without concomitant internucleosomal degradation of DNA
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