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
Hauptverfasser: Johnson, Betty H., Ayala-Torres, Sylvette, Chan, Lee-Nien L., El-Naghy, Mohamed, Thompson, E.Brad
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container_end_page 45
container_issue 1
container_start_page 35
container_title The Journal of steroid biochemistry and molecular biology
container_volume 61
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 &lt;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. 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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 &lt;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. 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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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