Vaughn J P, Davis P L, Jarboe M D, Huper G, Evans A C, Wiseman R W, Berchuck A, Iglehart J D, Futreal P A, Marks J R
Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA.
Cell Growth Differ. 1996 Jun;7(6):711-5.
Insight into the function of the BRCA1 tumor suppressor gene may be gained by studying its regulation. In this study, the expression of BRCA1 was examined as a function of the cell cycle in normal and tumor-derived breast epithelial cells. Cells arrested in G(zero) or early in G1 contained low levels of BRCA1 mRNA. After release, populations of cells reached maximal levels of BRCA1 in late G1 and S phase. Induction of BRCA1 was shown to occur before the onset of DNA synthesis by synchronizing cells at the G1-S boundary. Levels of the BRCA1 protein were regulated in a similar manner. No difference was observed between primary cultures of normal mammary epithelial cells and immortalized tumor-derived cell lines. These results suggest that BRCA1 may function at the G1-S checkpoint.
通过研究BRCA1肿瘤抑制基因的调控机制，或许可以深入了解其功能。在本研究中，我们检测了正常乳腺上皮细胞和肿瘤来源的乳腺上皮细胞中BRCA1的表达随细胞周期的变化情况。停滞于G（零）期或G1早期的细胞中BRCA1 mRNA水平较低。解除停滞状态后，细胞群体在G1晚期和S期达到BRCA1的最高水平。通过将细胞同步于G1-S边界，发现BRCA1的诱导发生在DNA合成开始之前。BRCA1蛋白水平也以类似方式受到调控。在正常乳腺上皮细胞的原代培养物和永生化肿瘤来源细胞系之间未观察到差异。这些结果表明，BRCA1可能在G1-S检查点发挥作用。
