According to a research from Weill Cornell Medicine and the Dana-Farber Cancer Institute, a protein called CDC7, who is thought to play an important role early in cell division, is in fact resupplyable by another protein called CDK1. This discovery represents a significant breakthrough in cell biology and may lead to new cancer therapies, because cancers often alter the molecular machinery of cell division to maintain their rapid growth.
Thestudy, which was first published on May 4 in Nature, analyzed the effects of eliminating CDC7 in a variety of mammalian cell types, a process that has been difficult to achieve. Effective cancer treatment options may be sighted simultaneously.
Specifically, this study provides an insight into one of the most important steps in cell division and suggests a new set of targets for future cancer therapies, according to Dr. Tobias Meyer, the Professor of Cell and Developmental Biology at the University of New York, who is a member of theSandra and Edward Meyer Cancer Centerat Weill Cornell Medicine.
Dr. Peter Sicinski, a Harvard Medical School teacher and a researcher at the Dana-Farber Cancer Institute, is the other co-senior author of the study, and the first authors are Dr. Jan Suski, a postdoctoral fellow in the Sicinski Lab at Dana-Farber, and Nalin Ratnayeke, a senior graduate student at Weill Cornell Medicine.
The cell cycle is a major component of biology. In recent decades, a large number of molecules have begun and controlled this process, including the signaling proteins CDK1, CDK4, CDK6, and CDC7. Much is already known about how these proteins are involved in cell division, and cancer drugs that are already in use. However, CDK1 and CDC7''s cell cycle roles have been somewhat murky.
CDC7 was thought to be crucial for a key initial step in cell divisionmoving the cell from the preparatory phase of the cell cycle, called G1, into the S phase, wherein the cell duplicates its DNA and becomes committed to division.
In a recent study, researchers used a variety of new and established protein-removal methods to create a surprising conclusion. Supposedly, deleting the mouse version of CDC7 in several cell types may slow or stop cell division, but only for a day or two before cell division resumes. Cells in mice, and presumably in all mammals, can compensate for the loss of CDC7 as a result of increased activity from CDK1even though the latter is structurally very different from CDC7 and
The findings highlight the complex molecular orchestration of the cell cycle, and suggest that simultaneously blocking CDC7 and CDK1 might be a powerful new strategy against cancer. The researchers are now continuing to investigate the roles of the different molecular actors in the cell cycle.
This paper demonstrates the extraordinary fact that cells can irgendwann redundancy for a given function with two very different levels of protein, not just with two closely related proteins, as were used to seeing.