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Growth factor modulation of metastatic lung colonization
S E Egan1, L Jarolim, S Rogelj
1Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.
Anticancer Research
|September 1, 1990
Summary
Growth factors influence tumor spread. Basic fibroblast growth factor (bFGF) inhibited metastasis, while colony-stimulating factor-1 (CSF-1) either stimulated or inhibited it, depending on cell conditions.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Altered growth factor signaling is implicated in neoplasia.
- The role of growth factors in tumor dissemination remains largely uncharacterized.
Purpose of the Study:
- To investigate the impact of growth factors on metastatic lung colonization.
- To elucidate how specific growth factors modulate the metastatic phenotype.
Main Methods:
- Utilized NIH-3T3 and C3H-10T 1/2 cell lines transformed with oncogenes (ras, src, v-fms).
- Administered exogenous basic fibroblast growth factor (bFGF) and colony-stimulating factor-1 (CSF-1).
- Assessed metastatic lung colonization following intravenous injection and evaluated autocrine conditioning effects.
Main Results:
- Autocrine bFGF, with a signal peptide, induced a metastatic phenotype in NIH-3T3 cells.
- Exogenous bFGF potently inhibited metastasis in ras- and src-transformed cells.
- CSF-1 stimulated metastasis in v-fms-transformed cells, but this effect was inhibited after autocrine medium conditioning.
Conclusions:
- Specific growth factors can significantly regulate tumor metastasis.
- The effect of growth factors (stimulatory or inhibitory) depends on the oncogenes driving transformation and cellular context (autocrine conditioning).