VEGFR2 Activates the GEP100-Arf6-AMAP1-Cortactin Pathway to Promote Angiogenesis
Author Information
Author(s): Hashimoto Ari, Hashimoto Shigeru, Ando Ryo, Noda Kosuke, Ogawa Eiji, Kotani Hirokazu, Hirose Mayumi, Menju Toshi, Morishige Masaki, Manabe Toshiaki, Toda Yoshinobu, Ishida Susumu, Sabe Hisataka
Primary Institution: Hokkaido University Graduate School of Medicine
Hypothesis
The GEP100-Arf6-AMAP1-cortactin pathway is activated by VEGFR2 to promote angiogenesis.
Conclusion
The GEP100-Arf6-AMAP1-cortactin pathway is essential for angiogenesis and can be targeted to inhibit cancer invasion and metastasis.
Supporting Evidence
- VEGF stimulation activates Arf6 in endothelial cells.
- GEP100 is necessary for VEGF-induced Arf6 activation.
- Knockdown of GEP100 or AMAP1 significantly impairs angiogenic activities.
- P4-TAT peptide blocks VEGF-induced angiogenesis.
- Components of the GEP100-Arf6-AMAP1-cortactin pathway are highly expressed in pathologic angiogenesis.
Takeaway
This study shows that a specific pathway in cells helps them grow new blood vessels, which is important for cancer growth.
Methodology
The study involved experiments with human umbilical vein endothelial cells (HUVECs) and various assays to measure angiogenic activities.
Limitations
The study primarily focuses on in vitro and animal models, which may not fully replicate human conditions.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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