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Titolo:
Suppression of c-myc expression and c-Myc function in response to sustained DNA damage in MCF-7 breast tumor cells
Autore:
Magnet, KJ; Orr, MS; Cleveland, JL; Rodriguez-Galindo, C; Yang, H; Yang, CY; Di, YM; Jain, PT; Gewirtz, DA;
Indirizzi:
Virginia Commonwealth Univ, Med Coll Virginia, Dept Med, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol Toxicol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA St Jude Childrens Hosp, Dept Biochem, Memphis, TN 38105 USA St Jude Childrens Hosp Memphis TN USA 38105 iochem, Memphis, TN 38105 USA
Titolo Testata:
BIOCHEMICAL PHARMACOLOGY
fascicolo: 5, volume: 62, anno: 2001,
pagine: 593 - 602
SICI:
0006-2952(20010901)62:5<593:SOCEAC>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANS-RETINOIC ACID; NORMAL P53 STATUS; INDUCED APOPTOSIS; CANCER-CELLS; ORNITHINE DECARBOXYLASE; IONIZING-RADIATION; GROWTH ARREST; GENE-EXPRESSION; DOWN-REGULATION; STRAND BREAKS;
Keywords:
MCF-7; VM-26 (teniposide); DNA damage; c-Myc; ornithine decarboxylase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Gewirtz, DA Virginia Commonwealth Univ, Med Coll Virginia, Dept Med, POB 980230, Richmond, VA 23298 USA Virginia Commonwealth Univ POB 980230 Richmond VA USA 23298 SA
Citazione:
K.J. Magnet et al., "Suppression of c-myc expression and c-Myc function in response to sustained DNA damage in MCF-7 breast tumor cells", BIOCH PHARM, 62(5), 2001, pp. 593-602

Abstract

The topoisomerase II inhibitors teniposide (VM-26), doxorubicin, and amsacrine (m-AMSA), as well as ionizing radiation, induce a transient suppression of c-myc mRNA, which correlates with growth inhibition of MCF-7 breast tumor cells. To further assess the involvement of c-myc in the DNA damage-induced signal transduction pathways of the breast tumor cell, we determined the influence of sustained DNA damage on c-myc expression, c-Myc protein levels and c-Myc function. Continuous exposure of MCF-7 breast tumor cells to VM-26 induced DNA strand breaks that were sustained for at least 9 hr. DNA strand breakage was accompanied by a decline in c-myc transcripts and c-Mycprotein levels by >90% after VM-26 exposure for 24 hr. The activity of a transcriptional target of the c-Myc protein, ornithine decarboxylase, was reduced by approximately 75% within 9 hr of DNA damage, in parallel to the declines in c-myc mRNA and protein levels. Extended exposure to VM-26 resulted in an initial loss of approximately 35% of the cell population followed by the death of additional cells such that by 72 hr only 50% of the cells were viable. Although apoptosis was evident 72 hr after initiating drug exposure [based on cell cycle analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assays, and an assessment of cell morphology], the primary phase of cell killing, which occurred during the first 24 hr was non-apoptotic. These studies indicate that non-apoptotic, pathways can also mediate cell death in the breast tumor cell and support the role of c-myc expression, c-Myc protein, and c-Myc function as elements of the DNA damage response pathway in the breast tumor cell. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:29:02