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The product of the v-src-inducible gene nr-13 is a potent anti-apoptotic factor
M Mangeney1, J R Schmitt, Y Leverrier
1Immunologie Cellulaine, Ecole normale supérieure de Lyon, France.
Abstract:
Tumorigenesis can be induced either by activating cell proliferation or by inhibiting metabolic pathways regulating programmed cell death (apoptosis). There is evidence suggesting that p60(v-src) and other tyrosine kinases protect cells against apoptosis. This effect could contribute to cell transformation by the Rous sarcoma virus. Mechanism of cell death inhibition by p60(v-src) remains largely unknown. We have recently reported that in avian cells p60(v-src) activates the expression of nr-13, a bcl-2-related gene. In this paper, we demonstrate, using the bone marrow derived cell line Baf-3 as an experimental model, that the product of this avian gene (nr-13) is a potent anti-apoptotic factor. In addition, we report that, in quail neuroretinal cells, nr-13 expression is activated upon infection by the Rous sarcoma virus (RSV) but not by other oncogenic retroviruses like FSV or MH2, suggesting that nr-13 is a specific target of v-src. Activation of nr-13 expression may be a key step in cellular transformation by v-src.
Insights
The Rous sarcoma virus (RSV) oncogene p60(v-src) protects cells from apoptosis by activating the nr-13 gene. This activation of nr-13, a bcl-2-related gene, is a key step in RSV-induced tumorigenesis.
Area of Science:
- Oncology
- Molecular Biology
- Virology
Background:
- Tumorigenesis involves altered cell proliferation and apoptosis regulation.
- p60(v-src) tyrosine kinase and related kinases are implicated in protecting cells from apoptosis.
- The precise mechanism by which p60(v-src) inhibits apoptosis is not fully understood.
Purpose of the Study:
- To investigate the role of the avian gene nr-13 in apoptosis inhibition.
- To determine if nr-13 is a target of p60(v-src) and contributes to cell transformation.
- To elucidate the mechanism of p60(v-src)-mediated anti-apoptotic effects.
Main Methods:
- Utilized the Baf-3 cell line as a model system.
- Assessed the anti-apoptotic function of the avian nr-13 gene product.
- Examined nr-13 expression in quail neuroretinal cells upon infection with Rous sarcoma virus (RSV) and other oncogenic retroviruses.
Main Results:
- Demonstrated that the avian nr-13 gene product acts as a potent anti-apoptotic factor.
- Showed that nr-13 expression is activated by Rous sarcoma virus (RSV) infection in quail neuroretinal cells.
- Observed that nr-13 expression is not activated by other oncogenic retroviruses (FSV, MH2), indicating specificity for v-src.
Conclusions:
- nr-13 functions as a significant anti-apoptotic factor.
- Activation of nr-13 expression by p60(v-src) is a specific event.
- nr-13 activation is a crucial mechanism in v-src-mediated cellular transformation and tumorigenesis.