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Expression of DNA polymerase {beta} cancer-associated variants in mouse cells results in cellular transformation.

Abstract：

:Thirty percent of the 189 tumors studied to date express DNA polymerase beta variants. One of these variants was identified in a prostate carcinoma and is altered from isoleucine to methionine at position 260, within the hydrophobic hinge region of the protein. Another variant was identified in a colon carcinoma and is altered at position 289 from lysine to methionine, within helix N of the protein. We have shown that the types of mutations induced by these cancer-associated variants are different from those induced by the wild-type enzyme. In this study, we show that expression of the I260M and K289M cancer-associated variants in mouse C127 cells results in a transformed phenotype in the great majority of cell clones tested, as assessed by focus formation and anchorage-independent growth. Strikingly, cellular transformation occurs after a variable number of passages in culture but, once established, does not require continuous expression of the polymerase beta variant proteins, implying that it has a mutational basis. Because DNA polymerase beta functions in base excision repair, our results suggest that mutations that arise during this process can lead to the onset or progression of cancer.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Sweasy JB,Lang T,Starcevic D,Sun KW,Lai CC,Dimaio D,Dalal S

doi

10.1073/pnas.0505166102

keywords:

subject

Has Abstract

pub_date

2005-10-04 00:00:00

pages

14350-5

issue

40

eissn

0027-8424

issn

1091-6490

pii

0505166102

journal_volume

102

pub_type

杂志文章

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