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The mouse int-2 gene exhibits basic fibroblast growth factor activity in a basic fibroblast growth factor-responsive
G R Merlo1, B J Blondel, R Deed
1Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland 20892.
Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|October 1, 1990
Summary
The int-2 protein can replace basic fibroblast growth factor (bFGF) in promoting adrenal tumor cell growth. Modifying int-2 with a signal peptide enabled it to support anchorage-independent growth and bind to bFGF receptors.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- The int-2 protein shares sequence homology with basic fibroblast growth factor (bFGF).
- SW13 adrenal cortical tumor cells require bFGF, interleukin 1, or transforming growth factor epsilon for anchorage-independent growth.
Purpose of the Study:
- To investigate the biological activity of the int-2 protein.
- To determine if int-2 can functionally substitute for bFGF in promoting SW13 cell growth.
Main Methods:
- Retroviral vectors encoding four variants of mouse int-2 cDNA were constructed.
- These vectors were introduced into human SW13 adrenal cortical tumor cells.
- Cellular growth in soft agar and conditioned medium activity were analyzed.
Main Results:
- Unmodified int-2 failed to induce SW13 cell growth in soft agar.
- A modified int-2 construct (pSP1) with a signal peptide enabled SW13 cell growth.
- Conditioned medium from pSP1-transfected cells supported SW13 growth and competed with bFGF for receptor binding.
Conclusions:
- The int-2 gene product can functionally replace bFGF in modulating anchorage-independent growth of SW13 cells.
- Signal peptide modification is crucial for int-2's biological activity in this context.