Analysis of common molecular mechanisms and pharmaceutical research in cancer invasion and angiogenesis

我们已经证明GEP100将EGFR信号与Arf6激活联系起来，从而诱导一些乳腺癌细胞的侵袭性活动。我们的分析表明，相同的GEP100-Arf6-AMAP1通路对于vegf诱导的血管生成活性是必不可少的，并且VEGFR2通过磷酸化tyr951结合到GEP100的PH结构域，激活Arf6-AMAP1通路以诱导血管生成。此外，我们还发现了抑制GEP100和VEGFR-2相互作用的小化合物。由受体酪氨酸激酶激活的GEP100-Arf6-AMAP1通路似乎在血管生成和癌症侵袭中很常见，并从病理分析中提供了新的治疗靶点。

We have shown that GEP100 links EGFR signaling to Arf6 activation to induce invasive activities of some breast cancer cells. Our analyses demonstrate that the same GEP100-Arf6-AMAP1 pathway is essential for VEGF-induced angiogenesis activities, and that VEGFR2, via phospho-Tyr951, binds to the PH domain of GEP100 to activate the Arf6-AMAP1 pathway to induce angiogenesis. Moreover, we found the small compound that inhibits the interaction between GEP100 and VEGFR-2. The GEP100-Arf6-AMAP1 pathway, activated by receptor tyrosine kinases, appears to be common in angiogenesis and cancer invasion, and provide their new therapeutic targets from a pathological analysis.