Luminal STAT5 mediates H2AX promoter activity in distinct population of basal mammary epithelial cells.

ABSTRACT: Deregulated STAT5 activity in the mammary gland causes parity-dependent tumorigenesis. Epithelial cell cultures transfected with constitutively active STAT5 express higher levels of the histone H2AX than their non-transfected counterparts. Higher H2AX expression may be involved in tumorigenesis. Here, we aimed to link high STAT5 activity to H2AX-GFP expression by looking for distinct types of mammary cells that express these proteins. In vitro and in transgenic mice, only 0.2 and 0.02%, respectively, of the cells expressed the H2AX-GFP hybrid gene. Its expression correlated with that of the endogenous H2AX gene, suggesting that detectable H2AX-GFP expression marks high levels of H2AX transcript. Methylation of the H2AX promoter characterized non-GFP-expressing H2AX-GFP cells and was invers

SUBMITTER: Reichenstein M 

PROVIDER: S-EPMC5173096 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature