2019
DOI: 10.3390/genes10030244
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Abstract: Promotion of the cell cycle is a major oncogenic mechanism of the oncogene c-MYC (MYC). MYC promotes the cell cycle by not only activating or inducing cyclins and CDKs but also through the downregulation or the impairment of the activity of a set of proteins that act as cell-cycle brakes. This review is focused on the role of MYC as a cell-cycle brake releaser i.e., how MYC stimulates the cell cycle mainly through the functional inactivation of cell cycle inhibitors. MYC antagonizes the activities and/or the e… Show more

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Cited by 141 publications
(102 citation statements)
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References 241 publications
(334 reference statements)
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“…It is clear that c-Myc expression levels tightly relate to cell proliferation. Many reports show c-Myc downregulation inhibits cell cycle progression through regulating transcriptional activation of target genes such as Cyclin D2 and Cyclin E1 and E2F1, while stimulating p21 activity and suppressing DNA replication [39][40][41]. In our study, NL-101 arrested cells at G0/G1 phase at higher concentration while inducing S phase arrest at lower concentration; this was accompanied by reduction of c-Myc and induction of CDK2, Cyclin E1, and p21.…”
Section: Discussionsupporting
confidence: 56%
“…It is clear that c-Myc expression levels tightly relate to cell proliferation. Many reports show c-Myc downregulation inhibits cell cycle progression through regulating transcriptional activation of target genes such as Cyclin D2 and Cyclin E1 and E2F1, while stimulating p21 activity and suppressing DNA replication [39][40][41]. In our study, NL-101 arrested cells at G0/G1 phase at higher concentration while inducing S phase arrest at lower concentration; this was accompanied by reduction of c-Myc and induction of CDK2, Cyclin E1, and p21.…”
Section: Discussionsupporting
confidence: 56%
“…This revealed select transcriptional regulators whose activity correlated with distinct cell cycle phase scores in both species (p < 0.01, Figure 3B-C ). Crucially, phase-specific activity aligned with previous studies of these regulators and the cell cycle; KLF5 accelerates mitotic entry and promotes cell proliferation by accelerating G2/M progression 26 , BRCA1 regulates key effectors controlling the G2/M checkpoint 27 , PTTG is active in G2/M phase 28 , MYCN stimulates cell cycle progression by reducing G1 phase 29 , Nr5a2/Lrh-1 knockdown leads to G1 arrest 30, 31 , Myc is a potent inductor of the transition from G1 to S-phase 32 , and Sox2 is a mitotic bookmarking transcription factor active at the M/G1 phase 33 . Notably, E2F1 was found active in G2/M phase of human HEK293 cells and at S-phase of mouse 3T3 cells.…”
Section: Resultssupporting
confidence: 57%
“…Interestingly, one cluster associated with TBK1 did not appear in the higher threshold analysis and demonstrated a clear decrease in as a function of dose ( Figure S20). Lastly, a major oncogene MYC [68,69] did not show up in the higher threshold analysis, whereas in this analysis MYC was clearly being activated with increasing dose ( Figure S20), indicating that space radiation exposure would increase the potential for carcinogenesis.…”
Section: Gsea C6: Oncogenic Signaturesmentioning
confidence: 79%