The c-Fes protein tyrosine kinase as a potential anti-angiogenic target in cancer
The c-Fes protein tyrosine kinase as a potential anti-angiogenic target in cancer
复制标题
DOI：
10.2741/3732
复制
发表时间：
2011-01-01
影响因子：
3.1
通讯作者：
Miyata, Yasuyoshi
中科院分区：
文献类型：
--
作者：
Kanda, Shigeru;Miyata, Yasuyoshi
血管生成与许多病理情况有关，包括癌症进展。新的方法使我们能够理解血管生成过程中内皮细胞过程是如何在体内被调节的。血管生成的关键因子是血管内皮生长因子(VEGFs)和Notch配体。然而，其他促血管生成因子在体内对血管生成的反应机制还很不清楚。利用培养的内皮细胞进行的研究表明，c-Fes参与了多种细胞因子受体下游的磷脂酰肌醇3-激酶(PI3-Kinase)的激活。PI3-K/c-Akt通路在血管生成过程中调节细胞的存活、迁移和内皮细胞的形态分化，c-Fes因此可能成为抗癌治疗的潜在靶点，尤其是对抗血管内皮生长因子难治性癌症患者。此外，许多实验表明，骨髓来源的单核细胞系调节血管生成，c-Fes也在这些细胞中表达。C-Fes在血管生成中的作用将是未来广泛研究的重点。
Angiogenesis is implicated in many pathological conditions, including cancer progression. Novel approaches have enabled an understanding of how endothelial cellular processes are regulated in vivo during angiogenesis. Key players in angiogenesis are vascular endothelial growth factors (VEGFs) and Notch ligands. However, mechanisms of angiogenic responses by other proangiogenic factors in vivo are largely unknown. Research using cultured endothelial cells has shown that c-Fes is involved in the activation of phosphoinositide 3-kinase (PI3-kinase) downstream of a variety of cytokine receptors. The PI3-kinase/c-Akt pathway regulates cell survival, migration, and morphological differentiation of endothelial cells during angiogenesis, and c-Fes thus may be a potential target of anti-cancer therapy, especially for patients with anti-VEGF refractory cancer. In addition, a number of experiments have shown that a bone marrow-derived monocytic lineage regulates angiogenesis, and c-Fes is also expressed in these cells. Roles for c-Fes during angiogenesis will be the focus of extensive research in the future.