Mouse fibrosarcoma VEGFWT (Control) Cell Line
- Name Gillian Tozer
- Institute Cancer Research UK, London Research Institute: Lincoln's Inn Fields
Tool name: Mouse fibrosarcoma VEGFWT (Control) Cell Line
Alternate names: VEGF-A, VEGF12, VEGF164, VEGF188
Tool type: Cell Lines
Tool sub-type: Continuous
Parental cell line: MEF
Description: Mouse fibrosarcoma cell lines that are capable of expressing all vascular endothelial growth factor (VEGF) isoforms (control) or only single isoforms of VEGF (VEGF120, VEGF164, or VEGF188) were developed under endogenous VEGF promoter control.
Using Cre/Lox technology, mice expressing all or only single isoforms of VEGF, known as Vegfa120/120, Vegfa164/164, and Vegfa188/188 mice were developed. Primary fibroblasts were isolated from mouse embryos that were produced by heterozygous breeding pairs of mice expressing single or all isoforms of vascular endothelial growth factor-A (VEGF-A) on Swiss background. Fibroblasts were immortalized and oncogenically transformed by retroviral transduction with SV40 and HRAS (characterised in Tozer et al., 2008. Cancer Res; 68: (7)).
The original rationale for the development of these cell lines relates to the fact that tubulin-binding vascular-disrupting agents (VDA) are currently in clinical trials for cancer therapy but the factors that influence tumour susceptibility to these agents are poorly understood. Researchers evaluated the consequences of modifying tumour vascular morphology and function on vascular and therapeutic response to combretastatin-A4 3-O-phosphate (CA-4-P), which was chosen as a model VDA. The cell lines themselves could be potentially valuable for the commercial/pharmaceutical industry.
Research area: Cancer ; Cell Signaling & Signal Transduction ; Developmental Biology ; Drug Discovery & Development ; Metabolism
- For Research Use Only
- • Tozer et al. 2008. Cancer Res. 68(7):2301-11. PMID: 18381437.
- • Blood vessel maturation and response to vascular-disrupting therapy in single vascular endothelial growth factor-A isoform-producing tumors.