Retinoblastoma protein-initiated cellular growth arrest overcomes the ability of cotransfected wild-type p53 to induce apoptosis
2000
Retinoblastoma Protein and p53 Interaction in Cancer Cells
publication
Author Information
Author(s): Shinohara H, Zhou J, Yoshikawa K, Yazumi S, Ko K, Yamaoka Y, Mizukami T, Yoshida T, Akinaga S, Tamaoki T, Motoda H, Benedict W F, Takahashi R
Primary Institution: Graduate School of Medicine, Kyoto University
Hypothesis
The retinoblastoma gene (RB) can regulate p53-mediated apoptosis in cancer cells.
Conclusion
The growth-inhibitory function of RB can overcome the ability of wild-type p53 to induce apoptosis.
Supporting Evidence
- RB functions as a growth and tumor suppressor in HTB9 human bladder carcinoma cells.
- p53+/RB– cells were susceptible to apoptosis under various experimental conditions.
- p53+/RB+ cells were significantly resistant to apoptosis and exhibited efficient growth arrest.
- Tumorigenicity in nude mice was lost by exogenous expression of wild-type p53.
Takeaway
RB helps stop cancer cells from growing, even when p53, a protein that usually makes cells die, is present.
Methodology
The study involved transfecting wild-type p53 into human bladder carcinoma cells and assessing their response to apoptosis under various conditions.
Digital Object Identifier (DOI)
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