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首页> 外文期刊>Cellular Signalling >Cell adhesion and EGFR activation regulate EphA2 expression in cancer
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Cell adhesion and EGFR activation regulate EphA2 expression in cancer

机译：细胞粘附和EGFR激活调节EphA2在癌症中的表达

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EphA2 is frequently overexpressed in cancer, and increasing amounts of evidence show that EphA2 contributes to multiple aspects of the malignant character including angiogenesis and metastasis. Several aspects of the regulation and functional significance of EphA2 expression in cancer are still largely unknown. Here we show that the expression of EphA2 in in vitro cultured cells, is restricted to cells growing adherently and that adhesion-induced EphA2 expression is dependent upon activation of the epidermal growth factor receptor (EGFR), mitogen activated protein kinase kinase (MEK) and Src family kinases (SRC). Moreover, the results show that adhesion-induced EGFR activation and EphA2 expression is affected by interactions with extracellular matrix (ECM) proteins working as integrin ligands. Stimulation with the EphA2 ligand, ephrinA1 inhibited ERK phosphorylation and cancer cell viability. These effects were however abolished by activation of the EGF-receptor ligand system favoring Ras/MAPK signaling and cell proliferation. Based on our results, we propose a regulatory mechanism where cell adhesion induces EGFR kinase activation and EphA2 expression: and where the effect of ephrinA1 mediated reduction in cell viability by inhibiting EphA2 expression is overruled by activated EGFR in human cancer cells.
机译：EphA2在癌症中经常过表达，越来越多的证据表明EphA2有助于恶性特征的多个方面，包括血管生成和转移。 EphA2在癌症中表达的调节和功能意义的几个方面仍是未知之数。在这里，我们显示EphA2在体外培养细胞中的表达仅限于粘附生长的细胞，并且粘附诱导的EphA2表达取决于表皮生长因子受体（EGFR），促分裂原活化蛋白激酶（MEK）和Src家族激酶（SRC）。此外，结果表明粘附诱导的EGFR激活和EphA2表达受到与作为整合素配体起作用的细胞外基质（ECM）蛋白相互作用的影响。用EphA2配体刺激，ephrinA1抑制ERK磷酸化和癌细胞活力。然而，这些作用通过激活促进Ras / MAPK信号传导和细胞增殖的EGF-受体配体系统而被消除。根据我们的研究结果，我们提出了一种调控机制，其中细胞粘附诱导EGFR激酶激活和EphA2表达：而在人癌细胞中，活化的EGFR抑制了ephrinA1介导的通过抑制EphA2表达而导致细胞活力降低的作用。

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