Differential Expression of DNA Double-Strand Break Repair Proteins in Breast Cells
Abstract
Two mechanisms that repair DNA double-strand breaks in mammalian cells are homologous recombination and non-homologous DNA end-joining (NHEJ). Previous studies showed that a critical component of the NHEJ pathway, the DNA-activated protein kinase (DNA-PK), was poorly expressed in non-lactating (resting) breast tissue. Therefore, we proposed to identify the mechanisms responsible for regulating levels of non-homologous end-joining DNA repair components in human breast tissue and to measure the DNA double-strand break repair capacity of breast epithelial cells. We reexamined the expression of DNA-PK in human breast tissues by immuno-histochemistry and extended these studies to two other components of the NHEJ repair pathway, XRCC4 and DNA ligase IV, as well as three other DNA repair components NBS1, MRE11, and PCNA. In contrast to the original report, 90% of the epithelial cells in normal resting breast tissues from 10 different patients express both components of DNA-PK, DNAPKcs and Ku. These tissues also expressed XRCC4, DNA Ligase IV, NBS1, MRE11, and PCNA at similar levels. However, only PCNA was expressed in the stromal cells from the same tissues. Somewhat strong expression of DNA-PK was seen in epithelial cells. Surprisingly, however, only PCNA was detectable expressed in stromal cells from these same tissues.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2001
- Accession Number
- ADA396504
Entities
People
- Carl W. Anderson
- Mangala Tawde
Organizations
- Brookhaven National Laboratory