Co-expression of vascular endothelial growth factor (VEGF) and its receptors (flk-1 and flt-1) in hormone-induced mammary cancer in the Noble rat
1999
VEGF and Its Receptors in Mammary Cancer
publication
Evidence: moderate
Author Information
Author(s): Xie B, Tam N N C, Tsao S W, Wong Y C
Primary Institution: The University of Hong Kong
Hypothesis
In mammary cancer, VEGF regulates not only endothelial proliferation and angiogenesis but also the growth of cancer cells by an autocrine mechanism mediated through its receptors.
Conclusion
The study suggests that VEGF may act as an autocrine growth factor for mammary cancer cells.
Supporting Evidence
- Mammary cancer cells expressed high levels of VEGF and its receptors.
- Intense reactivities to VEGF, flt-1, and flk-1 were observed in invasive mammary carcinoma.
- Western blot analysis confirmed the increase in flk-1 and flt-1 proteins in induced mammary cancers.
- There was a correlation between high VEGF activity and Ki-67 expression.
- The Ki-67 indices in areas of strong and weak VEGF reactivities were 58.3% and 3.7% respectively.
- Strong flk-1 reactivity also correlated with Ki-67 expression.
- The Ki-67 indices for areas of strong and weak flk-1 reactivities were 53.9% and 3.1% respectively.
- Overexpression of VEGF and flk-1 is correlated with a high Ki-67 index.
Takeaway
This study found that a protein called VEGF helps breast cancer cells grow, not just the blood vessels around them.
Methodology
The study used a new animal model for breast cancer and employed double-labelling immunocytochemistry to investigate correlations between cellular proliferation and the expression of VEGF and its receptors.
Digital Object Identifier (DOI)
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