Journal
GENES
Volume 8, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/genes8060158
Keywords
MYC; genomic instability; chemoresistance; gamma H2AX
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Funding
- USA National Institutes of Health (NIH) [R01CA140379]
- Biochemistry and Molecular Biology Translational Pilot Research Award
- Georgia Cancer Center Postdoctoral Research Excellence Award
- Augusta University Biochemistry and Cancer Biology Graduate Program
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Cancer is associated with genomic instability and aging. Genomic instability stimulates tumorigenesis, whereas deregulation of oncogenes accelerates DNA replication and increases genomic instability. It is therefore reasonable to assume a positive feedback loop between genomic instability and oncogenic stress. Consistent with this premise, overexpression of the MYC transcription factor increases the phosphorylation of serine 139 in histone H2AX (member X of the core histone H2A family), which forms so-called gamma H2AX, the most widely recognized surrogate biomarker of double-stranded DNA breaks (DSBs). Paradoxically, oncogenic MYC can also promote the resistance of cancer cells to chemotherapeutic DNA-damaging agents such as cisplatin, clearly implying an antagonistic role of MYC in genomic instability. In this review, we summarize the underlying mechanisms of the conflicting functions of MYC in genomic instability and discuss when and how the oncoprotein exerts the contradictory roles in induction of DSBs and protection of cancer-cell genomes.
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