Influence of amsacrine (m-AMSA) on bulk and gene-specific DNA damage and c-myc expression in MCF-7 breast tumor cells
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Cited by (29)
A cell competition–based small molecule screen identifies a novel compound that induces dual c-Myc depletion and p53 activation
2021, Journal of Biological ChemistryCitation Excerpt :Collectively, these data demonstrate that DJ34 is a DNA intercalator and a strong inhibitor of topo II, but not topo I. It has previously been shown that intron 1 of the c-MYC gene contains a sequence that reduces c-MYC transcription because of torsional tension that arises during transcription, and the activity of topo II is essential for relieving this tension and maintaining high levels of c-MYC transcription; indeed, expression of plasmid-encoded c-MYC complementary DNA lacking this intron does not require topo II activity (37–40). We analyzed c-Myc levels in the MIA–PaCa GPS–Myc cell line (41), which contains the endogenous WT c-MYC alleles in addition to a randomly integrated dsRED–IRES–GFP–c-MYC construct (Fig. 6G).
Induction of G<inf>2</inf>/M arrest and inhibition of c-myc and p53 transcription by WP631 in Jurkat T lymphocytes
2002, Biochemical PharmacologyCitation Excerpt :The refractoriness of MCF-7 cells to apoptosis induced by doxorubicin [12,34] or WP631 [9] and the limited apoptosis observed in Jurkat T cells after 72 hr treatment agrees with finding that the transcription of c-myc was highly sensitive to nanomolar concentrations of WP631 (Fig. 8). There is a known association between the effects of some drugs on c-myc expression and the response to DNA damage in MCF-7 cells [12,34]. We recently reported a diminution in c-myc RNA levels, without apoptosis, in MCF-7 cells as a result of WP631 treatment [9].
Preferential damage to defined regions of genomic DNA by AT-specific anticancer drugs
2002, Advances in DNA Sequence-Specific AgentsSuppression of c-myc expression and c-Myc function in response to sustained DNA damage in MCF-7 breast tumor cells
2001, Biochemical PharmacologyCitation Excerpt :In agreement with this concept, c-Myc-induced pathways that regulate apoptosis and cell cycle progression can be separated pharmacologically by treating myeloid cells with cyclic AMP analogues [15]. Transient exposure of MCF-7 breast tumor cells to the topoisomerase II inhibitors VM-26, doxorubicin, and m-AMSA, or to ionizing radiation, produces an early concentration-dependent (and in the case of radiation, a dose-dependent) reduction in c-myc transcript levels [16–19]. Suppression of c-myc mRNA by VM-26 (as well as by ionizing radiation) is a transient effect [18,19], which may be related to the transient nature of DNA strand breaks induced by acute exposure to topoisomerase II inhibitors or ionizing radiation [20–23].