VEGF Signaling Pathway

The VEGF family of ligands (VEGF-A, -B, -C, and -D) and the placenta growth factor are critical mediators of tumor angiogenesis. Interactions of these factors with three tyrosine kinase receptors (VEGFR-1, -2, and -3) and two coreceptors [NRP-1 and -2] have all been well characterized on endothelial cells. The role of VEGF in vascular development is well demonstrated by the fact that heterozygous deletion of VEGF is embryonic lethal, primarily owing to the impaired formation of vascular structures. VEGF-targeted therapies are used to treat a variety of cancers, including colorectal cancer, non–small cell lung cancer, renal cell carcinoma, pancreatic neuroendocrine tumors, and glioblastoma.

The biology behind tumor-derived VEGF's regulation of the tumor vasculature and the functions of endothelial cells has been well characterized. Many studies indicate that VEGF has a direct effect on the survival and growth of multiple cancer cells, mostly through an autocrine signaling mechanism. Lee et al. showed that the depletion of VEGF or VEGFR1 in breast cancer cells led to reduced tumor cell survival and postulated that VEGF works as an intracellular autocrine or "intracrine" survival factor. The roles of VEGF-VEGFR signaling and the effects of inhibiting VEGF/VEGFR in a variety of cancers are quite complex. Recent studies of glioblastoma and pancreatic neuroendocrine tumors in mouse models have suggested that antiangiogenesis therapy may induce tumor invasiveness and increase metastasis. Similar results have been found in human breast cancer cells in mice.

Recently, therapeutics targeting VEGF has improved the therapy of several types of human cancer. Some new anti-VEGF therapeutics is being tested in clinical studies of multiple types of cancer. As some of these compounds selectively target single components of VEGF signaling, toxicity may be reduced. Moreover, the addition of therapeutics targeting molecular pathways of VEGF-independent angiogenesis or even non-angiogenic pathways to anti-VEGF therapeutics may further improve therapy. Nevertheless, some questions remain to be answered concerning the role of VEGF in tumor biology and angiogenesis. Thus, a more detailed knowledge about the molecular mechanisms involved in VEGF-signaling and possible predictive markers for a response to anti-VEGF therapy are needed to improve cancer treatment.

Creative Biogene is able to offer a variety of VEGF signaling pathway related products including stable cell lines, viral particles and clones for your drug discovery projects.

VEGF Signaling Pathway Product Panel

AKT1	AKT2	BAD	CDC42	HSPB1	KRAS
MAP2K1	MAP2K2	MAPK1	MAPK12	MAPK14	MAPK3
MAPKAPK3	NRAS	PIK3R1	PIK3R2	PIK3R3	PLA2G4A
PPP3CC	PRKCA	PTGS2	PTK2	RAF1	SRC
VEGFA

References:

Bhattacharya R, et al. Intracrine VEGF Signaling Mediates the Activity of Prosurvival Pathways in Human Colorectal Cancer Cells. Cancer Research, 2016, 76(10).
Koch S. Signal transduction by vascular endothelial growth factor receptors. Cold Spring Harbor Perspectives in Medicine, 2011, 2(7):a006502.
Waldner M J, Neurath M F. Targeting the VEGF signaling pathway in cancer therapy. Expert Opin Ther Targets, 2012, 16(1):5-13.

* For research use only. Not intended for any clinical use.

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