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v-erbA cooperates with bFGF in neuroretina cell transformation
1Cancer Research Institute, University of California, San Francisco 94143-0128.
Virology
|February 1, 1993
Summary
Oncogenes erbA and erbB influence cell transformation in chicken neuroretina cells. Nuclear oncogenes cooperate with erbA while maintaining growth factor responsiveness, unlike cytoplasmic oncogenes.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Oncogenes play critical roles in cellular transformation and cancer development.
- Basic fibroblast growth factor (bFGF) is a key regulator of cell growth and differentiation.
- Understanding oncogene cooperation with growth factors is crucial for cancer research.
Purpose of the Study:
- To investigate the transforming ability of erbA and erbB oncogenes in chicken neuroretina (CNR) cells.
- To determine the effect of basic fibroblast growth factor (bFGF) on oncogene-induced cell transformation.
- To explore how other oncogenes modulate the interaction between erbA and bFGF.
Main Methods:
- Transfection of CNR cells with various oncogenes (erbA, erbB, src, ras, mill raf, fos, myb-ets, myc).
- Assessment of cell transformation and growth factor responsiveness.
- Analysis of oncogene localization (cytoplasmic, membrane-bound, nuclear).
Main Results:
- erbA oncogene alone required bFGF for transformation; erbB and erbA+erbB transformed cells independently of bFGF.
- Cytoplasmic/membrane-bound oncogenes (src, ras, mill raf) cooperated with erbA but induced bFGF unresponsiveness.
- Nuclear oncogenes (fos, myb-ets, myc) cooperated with erbA, but cells remained responsive to bFGF.
Conclusions:
- The localization of cooperating oncogenes dictates bFGF responsiveness in transformed CNR cells.
- Cytoplasmic oncogenes may pre-activate the bFGF signal transduction pathway, leading to growth factor independence.
- This study provides insights into the complex interplay between oncogenes and growth factor signaling in cellular transformation.
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