A Variant of DNA Polymerase β Is Not Cancer Specific

• Published in: Journal of investigative surgery 2004-11, Vol.17 (6), p.327-331
• Main Authors: Bu, Dawei, Cler, Leslie R., Lewis, Cheryl M., Euhus, David M.
• Format: Article
• Language: English
• Subjects: breast cancer; Breast Neoplasms - enzymology; Breast Neoplasms - genetics; Cell Line, Tumor; Colorectal Neoplasms - enzymology; Colorectal Neoplasms - genetics; DNA Polymerase beta - genetics; DNA polymerase β; DNA Primers; DNA Replication; Exons; Female; Genetic Variation; Humans; Male; polymerase βΔ208-236; Recombination, Genetic; Reverse Transcriptase Polymerase Chain Reaction; Sequence Deletion; Testicular Neoplasms - enzymology; Testicular Neoplasms - genetics
• ISSN: 0894-1939; 1521-0553
• DOI: 10.1080/08941930490524372

DNA polymerase β (pol β) carries out base-excision repair (BER) required for DNA maintenance, replication, and recombination in eukaryotic cells. A variant characterized by a deletion of exon 11, an 87-bp region in the catalytic domain (pol β Δ 208-236), was previously described as a possible cause of genomic instability in cancer. The variant form was hypothesized to act in a dominant negative fashion, due to the fact that the variant inhibits the gap filling and DNA binding activities of the wild-type pol β protein. DNA polymerase β transcripts were analyzed in 8 breast cancer cell lines, snap-frozen benign breast tissues from 10 women, and lymphocytes from 10 normal controls, using reverse-transcription polymerase chain reaction (RT-PCR) and three separate primer pairs. The exon 10-12 splice site (variant) was identified using a primer designed to span the spliced exons and by sequencing RT-PCR products that included exon 10, exon 11 (if present), and exon 12. In all of the samples tested, we found both the wild-type and exon 11 87-bp deleted variant mRNAs expressed. We conclude that expression of the DNA polymerase β variant (pol β Δ 208-236) is ubiquitous and not breast cancer specific.