CELL-CYCLE CONTROL OF BRCA2

Identifying the conditions and kinetics of the induction of BRCA2 gene expression may implicate roles for the function of the tumor suppress or gene. In this study, expression of BRCA2 mRNA is shown to be regula ted by the cell cycle and associated with proliferation in normal and tumor-derived breast epithelial cells. Cells arrested in G(0) or early G(1) contained low levels of BRCA2 mRNA. After release into a prolife rating state, cells produced maximum levels of BRCA2 mRNA in late G(1) and the S-phase. Similar cell cycle control of BRCA2 was observed in fractions of exponentially growing cells isolated by centrifugal elutr iation. Expression of BRCA2 was shown to be independent of bulk DNA sy nthesis. In addition, the kinetics of BRCA2 mRNA up-regulation appeare d to be similar to those of BRCA1, suggesting that the two genes could be commonly controlled. These results imply that these two tumor supp ressor genes are utilized during growth and may have a protective role in cellular proliferation.