The RUNX family of transcription factors, including RUNX1, RUNX2, and RUNX3, are key regulators of development and can function as either tumor suppressors or oncogenes in cancer. Emerging evidence suggests that the dysregulation of RUNX genes can promote genomic instability in both leukemia and solid cancers by impairing DNA repair mechanisms. RUNX proteins control the cellular response to DNA damage by regulating the p53, Fanconi anemia, and oxidative stress repair pathways through transcriptional or non-transcriptional mechanisms. This review highlights the importance of RUNX-dependent DNA repair regulation in human cancers.
Keyphrases
- dna repair
- transcription factor
- dna damage
- oxidative stress
- dna damage response
- dna binding
- genome wide identification
- gene expression
- chronic kidney disease
- papillary thyroid
- endothelial cells
- ischemia reperfusion injury
- acute myeloid leukemia
- squamous cell carcinoma
- diabetic rats
- childhood cancer
- heat shock protein