A node between proliferation, apoptosis, and growth arrest

✍ Scribed by Mikhail V. Blagosklonny

• Book ID: 101298366
• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 61 KB
• Volume: 21
• Category: Article
• ISSN: 0265-9247
• DOI: 10.1002/(sici)1521-1878(199908)21:8<704::aid-bies10>3.0.co;2-5

✦ Synopsis

Paradoxically, oncogenes and growth factors can induce proliferation and promote cellular survival but can also cause apoptosis and growth arrest. What determines whether a cell decides to proliferate, arrest growth, or die? Mitogens and activators of mitogen-activated pathways initiate the simultaneous production of proliferative (cyclins) and anti-proliferative (CDK inhibitors such as p21WAF1/ CIP1) signals. Quiescent cells may respond to these signals by proliferation whereas proliferating cells may respond by growth arrest. Although pro-apoptotic oncoproteins, which constitute the downstream pathway (cyclin D, E2F, c-myc) directly induce proliferation, the activation of the upstream steps (growth factor receptors, Ras, cytoplasmic kinases) is required to prevent apoptosis.