Role of VEGF-C in Proliferation and Migration in a Cancer Model

• Main Author: Benke, Emily Marie
• Format: Others
• Published: VCU Scholars Compass 2008
• Subjects: VEGFR3; VEGFR; cancer; tumor; Life Sciences; Physiology
• Online Access: http://scholarscompass.vcu.edu/etd/1533; http://scholarscompass.vcu.edu/cgi/viewcontent.cgi?article=2532&context=etd

Head and neck cancer ranks high among the most common cancers world wide. In addition, there is a high recurrence rate, as well as a high prevalence of loco-regional tumor spread. Among many factors contributing to metastasis is vascular endothelial cell growth factor C. VEGF-C is primarily an inducer of new lymph vessel formation, typically during embryogenesis; however, some advanced cancers show a significant increase in VEGF-C expression, suggesting a role in metastasis. In the current study, the effects of VEGF-C expression were tested in HN12 cells, which are highly metastatic and known to express high levels of the chemokine CXCL5. A connection between VEGF-C and CXCL5 expression was made in previous studies. VEGF-C expression was downregulated or upregulated in appropriate target cells, in order to test its effect on proliferation and migration. Downregulation of VEGF-C in HN12 cells resulted in a decrease in proliferation, migration and motility. Conversely, upregulation of VEGF-C in HN4 cells led to an increase in cell proliferation. In addition, downregulation of VEGF-C significantly lowered tumorigenicity in athymic mice. All results suggest VEGF-C is contributing to an increase in proliferation, migration and motility in this HNSCC model system.