Oncogenic cell cycle start control.
The ability to proliferate in the absence of anchorage is a fundamental attribute of cancer cells, yet how it is acquired is one central problem in cancer biology. By utilizing growth factor-transformable NRK cells and its insensitive mutants, we recently found that oncogenic stimulation invokes Cdk6 to participate in a critical step of the cell cycle start, but not via the regulation of its catalytic activity and that Cdk6 participation closely correlates with the anchorage-independent growth ability. Since many hematopoietic cells employ predominantly Cdk6 for the cell cycle start and perform anchorage-independent growth by nature, this finding raises the possibility that the mechanism by which oncogenic stimulation invokes anchorage-independent growth of NRK cells is similar to the one used for hematopoietic cell proliferation. We discuss this novel mechanism and its implication.
Jinno
S
S
Department of Biochemistry and Molecular Biology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, 113-0033, Tokyo, Japan.
Lin
J
J
Yageta
M
M
Okayama
H
H
D000818:Animals; D002448:Cell Adhesion; D002453:Cell Cycle / Q000235:genetics*; D002455:Cell Division; D051361:Cyclin-Dependent Kinase 6; D018844:Cyclin-Dependent Kinases; D005347:Fibroblasts / Q000166:cytology / Q000201:enzymology; D006801:Humans; D009857:Oncogenes; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*
D017346:Protein Serine-Threonine Kinases; C495911:CDK6 protein, human; D051361:Cyclin-Dependent Kinase 6; D018844:Cyclin-Dependent Kinases