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首页> 外文期刊>Biochimica et biophysica acta: international journal of biochemistry and biophysics >CD44 stimulation by fragmented hyaluronic acid induces upregulation and tyrosine phosphorylation of c-Met receptor protein in human chondrosarcoma cells.
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CD44 stimulation by fragmented hyaluronic acid induces upregulation and tyrosine phosphorylation of c-Met receptor protein in human chondrosarcoma cells.

机译：碎片透明质酸对CD44的刺激可诱导人软骨肉瘤细胞中c-Met受体蛋白的上调和酪氨酸磷酸化。

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摘要

Hepatocyte growth factor/scatter factor (HGF/SF) can induce proliferation and motility and promote invasion of tumor cells. Since HGF/SF receptor, c-Met, is expressed by tumor cells, and since stimulation of CD44, a transmembrane glycoprotein known to bind hyaluronic acid (HA) in its extracellular domain, is involved in activation of c-Met, we have studied the effects of CD44 stimulation by ligation with HA upon the expression and tyrosine phosphorylation of c-Met on human chondrosarcoma cell line HCS-2/8. The current study indicates that (a) CD44 stimulation by fragmented HA upregulates expression of c-Met proteins; (b) fragmented HA also induces tyrosine phosphorylation of c-Met protein within 30 min, an early event in this pathway as shown by the early time course of stimulation; (c) the effects of HA fragments are critically HA size-dependent. High molecular weight HA is inactive, but lower molecular weight fragments (M(r) 3.5 kDa) are active with maximal effect in the microg/ml range; (d) the standard form of CD44 (CD44s) is critical for the response because the effect on c-Met, both in terms of upregulation and phosphorylation, is inhibited by preincubation with an anti-CD44 monoclonal antibody; and (e) phosphorylation of c-Met induced by CD44 stimulation is inhibited by protein tyrosine kinase inhibitor, tyrphostin. Therefore, our study represents the first report that CD44 stimulation induced by fragmented HA enhances c-Met expression and tyrosine phosphorylation in human chondrosarcoma cells. Taken together, these studies establish a signal transduction cascade or cross-talk emanating from CD44 to c-Met.
机译：肝细胞生长因子/分散因子（HGF / SF）可以诱导增殖和运动并促进肿瘤细胞的侵袭。由于肿瘤细胞表达HGF / SF受体c-Met，并且由于刺激CD44（一种在细胞外域结合透明质酸（HA）的跨膜糖蛋白）参与c-Met的激活，因此我们进行了研究与HA连接刺激CD44对人软骨肉瘤细胞系HCS-2 / 8中c-Met表达和酪氨酸磷酸化的影响。当前的研究表明：（a）片段化HA刺激CD44上调c-Met蛋白的表达; （b）片段化的HA还可以在30分钟内诱导c-Met蛋白的酪氨酸磷酸化，这是该途径的早期事件，如刺激的早期过程所示; （c）HA片段的影响严重取决于HA大小。高分子量HA无活性，但低分子量片段（M（r）3.5 kDa）具有活性，在microg / ml范围内具有最大作用; （d）CD44（CD44s）的标准形式对于应答至关重要，因为与抗CD44单克隆抗体预孵育会抑制c-Met的上调和磷酸化作用; （e）蛋白质酪氨酸激酶抑制剂酪氨酸抑制蛋白抑制了CD44刺激引起的c-Met磷酸化。因此，我们的研究代表了第一个报道，由片段化HA诱导的CD44刺激可增强人软骨肉瘤细胞中c-Met表达和酪氨酸磷酸化。总之，这些研究建立了从CD44到c-Met的信号转导级联或串扰。

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