Tyrosine kinase activity of EphA2 promotes its S897 phosphorylation and glioblastoma cell proliferation
Tyrosine kinase activity of EphA2 promotes its S897 phosphorylation and glioblastoma cell proliferation
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DOI：
10.1016/j.bbrc.2018.04.020
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发表时间：
2018-05-23
影响因子：
3.1
通讯作者：
Katoh, Hironori
中科院分区：
文献类型：
--
作者：
Hamaoka, Yuho;Negishi, Manabu;Katoh, Hironori
EphA2是受体酪氨酸激酶Eph家族的成员，已报道通过丝氨酸897（S897）的磷酸化促进肿瘤恶性化。在这里，我们发现野生型EphA2的过表达通过ERK激活诱导5897磷酸化而没有生长因子或细胞因子，并促进胶质母细胞瘤细胞增殖。然而，EphA2的激酶失活突变体的过表达未能诱导ERK激活、S897磷酸化和促进胶质母细胞瘤细胞增殖。这些数据表明，当过表达时，EphA2通过其酪氨酸激酶活性诱导ERK活化，导致5897磷酸化并促进胶质母细胞瘤细胞增殖。我们的研究结果为EphA2如何介导胶质母细胞瘤进展提供了新的见解。(C)2018爱思唯尔公司All rights reserved.
EphA2, a member of the Eph family of receptor tyrosine kinases, has been reported to promote tumor malignancy through phosphorylation of serine 897 (S897). Here, we found that overexpression of wild type EphA2 induced 5897 phosphorylation through ERK activation without growth factors or cytokines and promoted glioblastoma cell proliferation. However, overexpression of a kinase-inactive mutant of EphA2 failed to induce ERK activation, S897 phosphorylation, and promotion of glioblastoma cell proliferation. These data suggest that when overexpressed, EphA2 induces ERK activation through its tyrosine kinase activity, leading to 5897 phosphorylation and promotion of glioblastoma cell proliferation. Our findings provide a new insight into how EphA2 mediates glioblastoma progression. (C) 2018 Elsevier Inc. All rights reserved.