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Updated: Jul 5, 2026
Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
Abrogation by c-myc of G1 phase arrest induced by RB protein but not by p53
1Center for Molecular Medicine, University of Texas Health Science Center, San Antonio 78245.
Abstract:
Inactivating mutations of the retinoblastoma gene (RB) are found in a wide variety of tumour cells. Replacement of wild-type RB can suppress the tumorigenicity of some of these cells, suggesting that the RB protein (Rb) may negatively regulate cell growth. As activation of c-myc expression promotes cell proliferation and blocks differentiation, it may positively regulate cell growth. The c-myc protein is localized in the nucleus and can physically associate with RB protein in vitro, hence c-myc may functionally antagonize RB function. Microinjection of Rb in G1 phase reversibly arrests cell-cycle progression. Here we co-inject RB protein with c-myc, EJ-ras, c-fos or c-jun protein. Co-injection of c-myc, but not EJ-ras, c-fos or c-jun, inhibits the ability of Rb to arrest the cell cycle. The c-myc does not inhibit the activity of another tumour supressor, p53 (ref. 12). Thus, c-myc and RB specifically antagonize one another in the cell.
Insights
Retinoblastoma (RB) protein normally halts cell growth. However, c-myc protein overrides this RB function, promoting cell proliferation. This study reveals a specific antagonism between c-myc and RB in cellular regulation.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Cycle Regulation
Background:
- Inactivating mutations in the retinoblastoma gene (RB) are common in various tumors.
- RB protein (Rb) acts as a tumor suppressor by negatively regulating cell growth.
- c-myc oncogene activation promotes cell proliferation and blocks differentiation, suggesting a positive growth regulatory role.
Purpose of the Study:
- To investigate the functional interaction between RB protein and c-myc.
- To determine if c-myc antagonizes the cell cycle-arresting function of RB.
- To explore the specificity of c-myc's interaction with RB in contrast to other oncoproteins.
Main Methods:
- Microinjection of purified RB protein into cells.
- Co-injection of RB protein with various oncoproteins, including c-myc, EJ-ras, c-fos, and c-jun.
- Assessment of cell-cycle progression following microinjection.
Main Results:
- Microinjection of RB protein alone caused reversible cell-cycle arrest in G1 phase.
- Co-injection of c-myc with RB inhibited RB's ability to arrest the cell cycle.
- Co-injection with EJ-ras, c-fos, or c-jun did not affect RB's cell-cycle arresting function.
- c-myc did not inhibit the tumor suppressor activity of p53.
Conclusions:
- c-myc specifically antagonizes the tumor-suppressive function of RB.
- This functional antagonism between c-myc and RB plays a role in cell proliferation and potentially tumorigenesis.
- The interaction highlights a key molecular mechanism in cell cycle control and cancer development.
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01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
02:36DNA Damage Can Stall the Cell Cycle