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 beta (P-pol) provides a rate-determining funct
ion during in vitro repair of abasic sites by one of the mammalian DNA base
excision repair pathways. Therefore, altered expression of beta-pol during
carcinogenesis could alter base excision repair and, consequently, be crit
ical to the integrity of the mammalian genome. We examined the expression o
f beta-pol in several cell lines and human adenocarcinomas using a quantita
tive immunoblotting method. In cell lines from normal breast or colon, the
level of beta-pol was similar to 1 ng/mg cell extract, whereas in all of th
e breast and colon adenocarcinoma cell lines tested, a higher level of beta
-pol was observed, In tissue samples, colon adenocarcinomas had a higher le
vel of beta-pol than adjacent normal mucosa. Breast adenocarcinomas exhibit
ed a wide range of beta-pol expression: one tumor had a much higher level o
f beta-pol (286 ng/mg cell extract) than adjacent normal breast tissue, whe
reas another tumor had the same level of beta-pol as adjacent normal tissue
. Differences in beta-pol expression level, from normal to elevated, were a
lso observed with prostate adenocarcinomas. All kidney adenocarcinomas test
ed had a slightly lower beta-pol level than adjacent normal tissue. This st
udy reveals that the base excision repair enzyme DNA polymerase beta is upr
egulated in some types of adenocarcinomas and cell lines, but not in others
.