Abstract
In the previous issue of Breast Cancer Research, Gardner and co-workers describe a novel interaction between Geminin, a protein that prevents reinitiation of DNA replication, and Topoisomerase IIα (TopoIIα), an enzyme essential for removing catenated intertwines between sister chromatids. Geminin facilitates the action of TopoIIα, thereby promoting termination of DNA replication at the same time it inhibits initiation. In this manner, Geminin ensures that cells duplicate their genome once, but only once, each time they divide. Remarkably, either depletion of Geminin or over-expression of Geminin inhibits the action of TopoIIα, thereby making Geminin an excellent target for cancer chemotherapy.
Highlights
In the previous issue of Breast Cancer Research, Gardner and co-workers describe a novel interaction between Geminin, a protein that prevents reinitiation of DNA replication, and Topoisomerase IIα (TopoIIα), an enzyme essential for removing catenated intertwines between sister chromatids
Since Geminin is selectively expressed in proliferating cells, and its level in cancer cells is markedly greater than in normal cells, it can be used as a biomarker for both the diagnosis and prognosis of cancer [8]
Working with human mammary epithelial (HME) cells, Gardner and colleagues [1] discovered that Geminin facilitates the ability of Topoisomerase IIα (TopoIIα) to bind chromatin and resolve catenated intertwines, and that this trimolecular interaction appears to be regulated by two protein kinases, one (CKIε) that activates TopoIIα, and one (Cdc7-Dbf4) that inhibits TopoIIα
Summary
In the previous issue of Breast Cancer Research, Gardner and co-workers describe a novel interaction between Geminin, a protein that prevents reinitiation of DNA replication, and Topoisomerase IIα (TopoIIα), an enzyme essential for removing catenated intertwines between sister chromatids. Geminin inhibition of Cdt1, is only one of five concerted pathways in metazoan cells that restrict nuclear DNA replication to one complete round per cell division, thereby maintaining genome stability and preventing cells from becoming aneuploid. Working with human mammary epithelial (HME) cells, Gardner and colleagues [1] discovered that Geminin facilitates the ability of Topoisomerase IIα (TopoIIα) to bind chromatin and resolve catenated intertwines, and that this trimolecular interaction appears to be regulated by two protein kinases, one (CKIε) that activates TopoIIα, and one (Cdc7-Dbf4) that inhibits TopoIIα.
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