Adding to the CASeload: unwarranted p53 signaling induced by Cas9.
Veronica RendoOana M EnacheUri Ben-DavidPublished in: Molecular & cellular oncology (2020)
We investigated the genetic and transcriptional changes associated with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated protein 9 (Cas9) expression in human cancer cell lines. For a subset of cell lines with a wild-type tumor protein TP53 (best known as p53), we detected p53 pathway activation, DNA damage accumulation and emerging p53-inactivating mutations following Cas9 introduction. We discuss the potential implications of our findings in basic and translational research.
Keyphrases
- genome editing
- crispr cas
- wild type
- dna damage
- endothelial cells
- poor prognosis
- genome wide
- papillary thyroid
- oxidative stress
- binding protein
- gene expression
- squamous cell
- transcription factor
- induced pluripotent stem cells
- protein protein
- dna methylation
- risk assessment
- pluripotent stem cells
- human health
- copy number
- atomic force microscopy
- long non coding rna
- young adults
- single molecule