DNA damage-induced cell cycle checkpoints involve both p53-dependent and -independent pathways: role of telomere repeat binding factor 2
2001
DNA Damage and Cell Cycle Checkpoints in Colon Cancer
publication
Author Information
Author(s): Narayan S, Jaiswal A S, Multani A S, Pathak S
Primary Institution: UF Shands Cancer Center and Anatomy and Cell Biology, College of Medicine, University of Florida, Gainesville, FL 32610
Hypothesis
How do DNA damage-induced cell cycle checkpoints operate in colon cancer cells?
Conclusion
The study found that DNA damage from MNNG leads to cell cycle arrest in colon cancer cells through both p53-dependent and independent pathways.
Supporting Evidence
- Treatment of colon cancer cells with MNNG causes DNA damage with reduced telomeric signals in a p53-dependent manner.
- Increased cell cycle arrest occurs in S-G2/M by both p53-dependent and independent mechanisms.
- Cellular levels of TRF2 may play a critical role in MNNG-induced cell cycle arrest and apoptosis of colon cancer cells.
Takeaway
When colon cancer cells are damaged, they can stop themselves from dividing, and this can happen in two different ways, one of which involves a protein called p53.
Digital Object Identifier (DOI)
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