DNA Repair in Colon Cancer Cell Lines.

Abstract

Colorectal cancer remains the third most common cancer world‐wide, despite recent advances in early diagnosis and following treatment strategies. Genome stability plays important role in cancer’s origin and progression. The fidelity of DNA repair is of most importance for the colorectal cancer, which characterized by accumulation of mutations in oncogenes and tumor suppressor genes, and dozens of so called “passenger” mutations in genes that are not driving cancer progression. Studying of cell cultures established from colon‐cancer patients are important tool for understanding molecular mechanisms behind cancerous transformation and drug development. Two colon‐cancer cell lines are widely used in such research are HT29 and HCT116. We analyzed the nucleotide excision repair (NER) in these cells by monitoring DNA repair following UV‐C exposure. The NER pathway is one of several fundamental repair mechanisms that is guarding genome from accumulation of DNA damage. Following the single gel electrophoresis technique, we determine that HT29 cells are slower at repairing UV‐C induced damage compared to HCT116 cells or normal human fibroblasts, HDFa cells. This is an important funding, because it shows that colon‐cancer cell lines are different in stress response capacity. Such difference might be important for the drug development and our understanding of basic mechanisms of genome stability in cancer cell lines.Support or Funding Information1) Research reported in this publication was supported by the National Institute Of General Medical Sciences of the National Institutes of Health under Award Numbers UL1GM118991, TL4GM118992, or RL5GM118990. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. UA is an AA/EO employer and educational institution and prohibits illegal discrimination against any individual: www.alaska.edu/titleIXcompliance/nondiscrimination. 2) NASA EPSCoR, NNH15ZHA003C