A long-standing question in cancer biology has been the extent to which DNA repair may be altered during the process of carcinogenesis. We have shown recently that DNA polymerase β (β-pol) provides a rate-determining function during in vitro repair of abasic sites by one of the mammalian DNA base excision repair pathways. Therefore, altered expression of β-pol during carcinogenesis could alter base excision repair and, consequently, be critical to the integrity of the mammalian genome. We examined the expression of β-pol in several cell lines and human adenocarcinomas using a quantitative immunoblotting method. In cell lines from normal breast or colon, the level of β-pol was ~ 1 ng/mg cell extract, whereas in all of the breast and colon adenocarcinoma cell lines tested, a higher level of β-pol was observed. In tissue samples, colon adenocarcinomas had a higher level of β-pol than adjacent normal mucosa. Breast adenocarcinomas exhibited a wide range of β-pol expression: one tumor had a much higher level of β-pol (286 ng/mg cell extract) than adjacent normal breast tissue, whereas another tumor had the same level of β-pol as adjacent normal tissue. Differences in β-pol expression level, from normal to elevated, were also observed with prostate adenocarcinomas. All kidney adenocarcinomas tested had a slightly lower β-pol level than adjacent normal tissue. This study reveals that the base excision repair enzyme DNA polymerase β is upregulated in some types of adenocarcinomas and cell lines, but not in others.
ASJC Scopus subject areas
- Cancer Research