DNA damage-induced cell cycle checkpoints involve both p53-dependent and -independent pathways: role of telomere repeat binding factor 2.
Treatment of colon cancer cells with MNNG causes DNA damage with reduced telomeric signals in a p53-dependent manner, but increased cell cycle arrest in S-G(2)/M by both p53-dependent and independent mechanisms. Results also indicate that cellular levels of TRF2 may play a critical role in MNNG-induced cell cycle arrest and apoptosis of colon cancer cells.
Narayan
S
S
UF Shands Cancer Center and Anatomy and Cell Biology, College of Medicine, University of Florida, Gainesville, FL 32610, USA.
Jaiswal
A S
AS
Multani
A S
AS
Pathak
S
S
D017209:Apoptosis; D015153:Blotting, Western; D002453:Cell Cycle / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000378:metabolism*; D004247:DNA / Q000378:metabolism; D004249:DNA Damage; D004268:DNA-Binding Proteins / Q000378:metabolism*; D005434:Flow Cytometry; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008769:Methylnitronitrosoguanidine / Q000633:toxicity*; D016133:Polymerase Chain Reaction; D035341:Telomeric Repeat Binding Protein 2; D014407:Tumor Cells, Cultured / Q000187:drug effects*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
D004268:DNA-Binding Proteins; D035341:Telomeric Repeat Binding Protein 2; D016159:Tumor Suppressor Protein p53; D008769:Methylnitronitrosoguanidine; D004247:DNA