Abstract
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.
Original language | English |
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Pages (from-to) | 23-29 |
Number of pages | 7 |
Journal | Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis |
Volume | 477 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 2001 Jun 2 |
Externally published | Yes |
Keywords
- Anchorage-independent
- Hematopoietic cell
- Oncogenic stimulation
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Health, Toxicology and Mutagenesis