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[Cancer cells escape from failsafe programs in a simple Twist]
Alain Puisieux1, Sandrine Valsesia-Wittmann
1Unité Inserm 590, Centre Léon Bérard, 28, rue Laennec, 69008 Lyon. puisieux@lyon.fnclcc.fr
Bulletin Du Cancer
|March 29, 2006
Summary
Oncogene cooperation between N-Myc and Twist 1 inhibits apoptosis, promoting neuroblastoma growth. Twist 1
Area of Science:
- Oncology and Developmental Biology
- Cancer Cell Biology
Background:
- Cellular senescence and apoptosis are critical barriers to abnormal cell proliferation.
- Oncogene-driven hyperproliferation requires concurrent inhibition of apoptosis for malignant outgrowth.
- Neuroblastoma, a common childhood cancer, exemplifies this process through N-Myc and Twist 1 cooperation.
Purpose of the Study:
- To elucidate the oncogenic cooperation between N-Myc and Twist 1 in neuroblastoma development.
- To explain the mechanism by which Twist 1 counteracts apoptosis induced by N-Myc.
- To highlight the role of embryogenesis regulators in human cancer.
Main Methods:
- Review of recent studies on N-Myc and Twist 1 in neuroblastoma.
- Analysis of the ARF/p53 pathway's regulation by Twist 1.
- Examination of Twist 1 overexpression in various human cancers.
Main Results:
- N-Myc drives cell proliferation, while Twist 1 inhibits apoptosis by downregulating the ARF/p53 pathway.
- This mechanism explains the infrequent p53 mutations observed in neuroblastomas.
- Twist 1 overexpression is frequently reported in diverse human cancers, suggesting a role in tumor progression.
Conclusions:
- The N-Myc and Twist 1 oncogenic partnership is crucial for neuroblastoma development by suppressing apoptosis.
- Twist 1's role in antagonizing the ARF/p53 pathway is key to malignant outgrowth.
- Twist 1 is implicated as a significant factor in the progression of various human cancers.
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