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Myc and the cell cycle
B Amati1, K Alevizopoulos, J Vlach
1Swiss Institute for Experimental Cancer Research (ISREC), CH-1066 Epalinges, Switzerland. bruno.amati@isrec.unil.ch
Frontiers in Bioscience : a Journal and Virtual Library
|February 27, 1998
Summary
The c-Myc oncoprotein drives cell cycle progression by activating cyclin-dependent kinases (CDKs) and inhibiting CDK inhibitors. Myc also promotes cell proliferation but can induce apoptosis without survival factors, linking its oncogenic activity to cell cycle control.
Area of Science:
- Molecular Biology
- Cell Cycle Regulation
- Oncogenesis
Background:
- The c-Myc oncoprotein is a key regulator of cell proliferation and a potent oncogene.
- Understanding Myc's role in cell cycle control is crucial for cancer research.
Purpose of the Study:
- To review recent advances in elucidating the molecular mechanisms by which Myc influences cell cycle progression.
- To explore the interplay between Myc, cyclin-dependent kinases (CDKs), and CDK inhibitors.
Main Methods:
- Review of existing literature on Myc function in cell cycle control.
- Analysis of molecular pathways involving Myc, cyclins, CDKs, and CDK inhibitors (e.g., p27Kip1, p21Cip1, p16INK4a).
Main Results:
- Myc promotes cell cycle entry by activating G1-specific CDKs, particularly cyclin E/CDK2.
- Myc inactivates CDK inhibitors (p27Kip1, p21Cip1) and induces Cdc25A phosphatase.
- Myc and cyclin E/CDK2 activity can decouple p16INK4a-mediated growth arrest from pRb pathway activation.
Conclusions:
- Myc is a potent mitogenic stimulus that regulates cell cycle progression through multiple pathways.
- Myc's ability to override cell cycle checkpoints and induce proliferation contributes to its oncogenic potential.
- Further exploration is needed on Myc's interaction with cyclin D/CDK4/6 and its role in cooperating with other oncogenes like Ras.