Glucocorticoid/oxysterol-induced DNA lysis in human leukemic cells
Both glucocorticoids and oxysterols, steroids with quite different known transduction pathways, cause the death of lymphoid cells. Dual TUNEL/propidium iodide assays on sensitive human leukemic CEM-C7 clones treated with either steroid were clearly positive by 48 h, consistent with apoptosis. Both s...
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Veröffentlicht in: | The Journal of steroid biochemistry and molecular biology 1997-04, Vol.61 (1), p.35-45 |
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creator | Johnson, Betty H. Ayala-Torres, Sylvette Chan, Lee-Nien L. El-Naghy, Mohamed Thompson, E.Brad |
description | Both glucocorticoids and oxysterols, steroids with quite different known transduction pathways, cause the death of lymphoid cells. Dual TUNEL/propidium iodide assays on sensitive human leukemic CEM-C7 clones treated with either steroid were clearly positive by 48 h, consistent with apoptosis. Both steroids evoked two distinctive types of DNA lysis: cleavage into large fragments of several different sizes and the classic “ladders”, multiples of ∼200 base pairs. Conventional gel electrophoresis showed that a small proportion of total DNA had undergone laddering 36–48 h after treatment with glucocorticoid or 24 h after oxysterol exposure. On field inversion gel electrophoresis of cellular DNA both steroids caused an increase in an array of large DNA fragments |
doi_str_mv | 10.1016/S0960-0760(96)00256-7 |
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Dual TUNEL/propidium iodide assays on sensitive human leukemic CEM-C7 clones treated with either steroid were clearly positive by 48 h, consistent with apoptosis. Both steroids evoked two distinctive types of DNA lysis: cleavage into large fragments of several different sizes and the classic “ladders”, multiples of ∼200 base pairs. Conventional gel electrophoresis showed that a small proportion of total DNA had undergone laddering 36–48 h after treatment with glucocorticoid or 24 h after oxysterol exposure. On field inversion gel electrophoresis of cellular DNA both steroids caused an increase in an array of large DNA fragments <50 kb in size. A 50 kb fragment appeared 36 h after treatment with either steroid, but only oxysterol treatment caused a significant increase in a 300 kb fragment. Oxysterol treatment did not result in DNA fragmentation in the resistant M10R5 subclone, which retained sensitivity to glucocorticoids. We conclude that glucocorticoids and oxysterols kill these cells with similar, but not identical, patterns of DNA lysis which occur just before or concomitant with the onset of cell death.</description><identifier>ISSN: 0960-0760</identifier><identifier>EISSN: 1879-1220</identifier><identifier>DOI: 10.1016/S0960-0760(96)00256-7</identifier><identifier>PMID: 9328208</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Antineoplastic agents ; Biological and medical sciences ; Cell Division ; Chemotherapy ; Dexamethasone - pharmacology ; DNA Fragmentation - drug effects ; DNA, Neoplasm - analysis ; Glucocorticoids - pharmacology ; Humans ; Hydroxycholesterols - pharmacology ; Medical sciences ; Pharmacology. Drug treatments ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology ; Tumor Cells, Cultured</subject><ispartof>The Journal of steroid biochemistry and molecular biology, 1997-04, Vol.61 (1), p.35-45</ispartof><rights>1997</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-4e199df4621868ca7231d23c735a479e194ae23e2b82ba87d3b2ce653cd7de463</citedby><cites>FETCH-LOGICAL-c420t-4e199df4621868ca7231d23c735a479e194ae23e2b82ba87d3b2ce653cd7de463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0960-0760(96)00256-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2812133$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9328208$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Johnson, Betty H.</creatorcontrib><creatorcontrib>Ayala-Torres, Sylvette</creatorcontrib><creatorcontrib>Chan, Lee-Nien L.</creatorcontrib><creatorcontrib>El-Naghy, Mohamed</creatorcontrib><creatorcontrib>Thompson, E.Brad</creatorcontrib><title>Glucocorticoid/oxysterol-induced DNA lysis in human leukemic cells</title><title>The Journal of steroid biochemistry and molecular biology</title><addtitle>J Steroid Biochem Mol Biol</addtitle><description>Both glucocorticoids and oxysterols, steroids with quite different known transduction pathways, cause the death of lymphoid cells. Dual TUNEL/propidium iodide assays on sensitive human leukemic CEM-C7 clones treated with either steroid were clearly positive by 48 h, consistent with apoptosis. Both steroids evoked two distinctive types of DNA lysis: cleavage into large fragments of several different sizes and the classic “ladders”, multiples of ∼200 base pairs. Conventional gel electrophoresis showed that a small proportion of total DNA had undergone laddering 36–48 h after treatment with glucocorticoid or 24 h after oxysterol exposure. On field inversion gel electrophoresis of cellular DNA both steroids caused an increase in an array of large DNA fragments <50 kb in size. A 50 kb fragment appeared 36 h after treatment with either steroid, but only oxysterol treatment caused a significant increase in a 300 kb fragment. Oxysterol treatment did not result in DNA fragmentation in the resistant M10R5 subclone, which retained sensitivity to glucocorticoids. We conclude that glucocorticoids and oxysterols kill these cells with similar, but not identical, patterns of DNA lysis which occur just before or concomitant with the onset of cell death.</description><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cell Division</subject><subject>Chemotherapy</subject><subject>Dexamethasone - pharmacology</subject><subject>DNA Fragmentation - drug effects</subject><subject>DNA, Neoplasm - analysis</subject><subject>Glucocorticoids - pharmacology</subject><subject>Humans</subject><subject>Hydroxycholesterols - pharmacology</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology</subject><subject>Tumor Cells, Cultured</subject><issn>0960-0760</issn><issn>1879-1220</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOwzAQRS0EKqXwCZWyQAgWoX4kdrJCpUBBqmABrC3XngpDEhc7QfTvcR_qlpUX98z4zkFoSPA1wYSPXnHJcYoFx5clv8KY5jwVB6hPClGmhFJ8iPp75BidhPCJMWaMiB7qlYwWFBd9dDutOu20863VzpqR-12FFryrUtuYToNJ7p7HSbUKNiS2ST66WjVJBd0X1FYnGqoqnKKjhaoCnO3eAXp_uH-bPKazl-nTZDxLdUZxm2ZAytIsMk5JwQutBGXEUKYFy1UmyphmCigDOi_oXBXCsDnVwHOmjTCQcTZAF9u9S---OwitrG1YN1ANuC5IEY-iJKf_giRWYDlfb8y3oPYuBA8LufS2Vn4lCZZryXIjWa4NypLLjWQp4txw90E3r8Hsp3ZWY36-y1XQqlp41Wgb9hgtSCzAInazxSBa-7HgZdAWmijdetCtNM7-U-QPoZ-Xkw</recordid><startdate>19970401</startdate><enddate>19970401</enddate><creator>Johnson, Betty H.</creator><creator>Ayala-Torres, Sylvette</creator><creator>Chan, Lee-Nien L.</creator><creator>El-Naghy, Mohamed</creator><creator>Thompson, E.Brad</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7X8</scope></search><sort><creationdate>19970401</creationdate><title>Glucocorticoid/oxysterol-induced DNA lysis in human leukemic cells</title><author>Johnson, Betty H. ; Ayala-Torres, Sylvette ; Chan, Lee-Nien L. ; El-Naghy, Mohamed ; Thompson, E.Brad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-4e199df4621868ca7231d23c735a479e194ae23e2b82ba87d3b2ce653cd7de463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Cell Division</topic><topic>Chemotherapy</topic><topic>Dexamethasone - pharmacology</topic><topic>DNA Fragmentation - drug effects</topic><topic>DNA, Neoplasm - analysis</topic><topic>Glucocorticoids - pharmacology</topic><topic>Humans</topic><topic>Hydroxycholesterols - pharmacology</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Johnson, Betty H.</creatorcontrib><creatorcontrib>Ayala-Torres, Sylvette</creatorcontrib><creatorcontrib>Chan, Lee-Nien L.</creatorcontrib><creatorcontrib>El-Naghy, Mohamed</creatorcontrib><creatorcontrib>Thompson, E.Brad</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Johnson, Betty H.</au><au>Ayala-Torres, Sylvette</au><au>Chan, Lee-Nien L.</au><au>El-Naghy, Mohamed</au><au>Thompson, E.Brad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucocorticoid/oxysterol-induced DNA lysis in human leukemic cells</atitle><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle><addtitle>J Steroid Biochem Mol Biol</addtitle><date>1997-04-01</date><risdate>1997</risdate><volume>61</volume><issue>1</issue><spage>35</spage><epage>45</epage><pages>35-45</pages><issn>0960-0760</issn><eissn>1879-1220</eissn><abstract>Both glucocorticoids and oxysterols, steroids with quite different known transduction pathways, cause the death of lymphoid cells. Dual TUNEL/propidium iodide assays on sensitive human leukemic CEM-C7 clones treated with either steroid were clearly positive by 48 h, consistent with apoptosis. Both steroids evoked two distinctive types of DNA lysis: cleavage into large fragments of several different sizes and the classic “ladders”, multiples of ∼200 base pairs. Conventional gel electrophoresis showed that a small proportion of total DNA had undergone laddering 36–48 h after treatment with glucocorticoid or 24 h after oxysterol exposure. On field inversion gel electrophoresis of cellular DNA both steroids caused an increase in an array of large DNA fragments <50 kb in size. A 50 kb fragment appeared 36 h after treatment with either steroid, but only oxysterol treatment caused a significant increase in a 300 kb fragment. Oxysterol treatment did not result in DNA fragmentation in the resistant M10R5 subclone, which retained sensitivity to glucocorticoids. We conclude that glucocorticoids and oxysterols kill these cells with similar, but not identical, patterns of DNA lysis which occur just before or concomitant with the onset of cell death.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>9328208</pmid><doi>10.1016/S0960-0760(96)00256-7</doi><tpages>11</tpages></addata></record> |
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subjects | Antineoplastic agents Biological and medical sciences Cell Division Chemotherapy Dexamethasone - pharmacology DNA Fragmentation - drug effects DNA, Neoplasm - analysis Glucocorticoids - pharmacology Humans Hydroxycholesterols - pharmacology Medical sciences Pharmacology. Drug treatments Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology Tumor Cells, Cultured |
title | Glucocorticoid/oxysterol-induced DNA lysis in human leukemic cells |
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