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Published on: December 31, 2014
E2F1 and c-Myc in cell growth and death
Itaru Matsumura1, Hirokazu Tanaka, Yuzuru Kanakura
1Department of Hematology/Oncology, Osaka University Graduate School of Medicine 2-2 Yamada-oka, Suita, Osaka 565-0871 Japan. matumura@bldon.med.osaka-u.ac.jp
Cell Cycle (Georgetown, Tex.)
|July 10, 2003
Summary
Cell cycle regulators c-Myc and E2F1 control cell growth and apoptosis. They influence cell death through transcription and by modulating signaling pathways like NF-kappaB.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- The cell cycle machinery governs cell proliferation, survival, and death.
- Key regulators like c-Myc and E2F1, involved in G1/S transition, can induce apoptosis.
- E2F1's role in apoptosis is supported by observations in deficient mouse models.
Purpose of the Study:
- To investigate the mechanisms by which c-Myc and E2F1 regulate cell death.
- To identify molecular mediators involved in c-Myc- and E2F1-induced apoptosis.
- To explore the interplay between c-Myc, E2F1, and signal transduction pathways in cell fate determination.
Main Methods:
- Analysis of gene expression and protein interactions.
- Utilizing knockout mouse models to assess apoptosis defects.
- Investigating the modulation of signaling pathways such as NF-kappaB.
Main Results:
- Overexpression of c-Myc or E2F1 can trigger apoptosis.
- Specific molecules like p14/p19ARF, ornithine decarboxylase, lactate dehydrogenase-A, p73, Apaf-1, and caspase-3 mediate c-Myc/E2F1-induced apoptosis.
- c-Myc and E2F1 were found to inhibit NF-kappaB activity, impacting responses to TNFalpha and reactive oxygen species.
Conclusions:
- c-Myc and E2F1 are critical regulators of both cell growth and cell death.
- These regulators exert control not only via transcriptional induction but also by modulating key signal transduction pathways.
- Understanding these pathways provides insights into cell fate decisions and potential therapeutic targets.
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