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首页> 外文期刊>Neoplasia: an international journal for oncology research >RhoC Mediates Epidermal Growth Factor-Stimulated Migration and Invasion in Head and Neck Squamous Cell Carcinoma
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RhoC Mediates Epidermal Growth Factor-Stimulated Migration and Invasion in Head and Neck Squamous Cell Carcinoma

机译：rhoc介导表皮生长因子刺激的迁移和侵袭头颈鳞状细胞癌

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Epidermal growth factor receptor (EGFR) is overexpressed in head and neck squamous cell carcinoma (HNSCC) where it has been shown to promote tumor cell invasion upon phosphorylation. One mechanism by which EGFR promotes tumor progression is by activating signal cascades that lead to loss of E-cadherin, a transmembrane glycoprotein of the cell-cell adherence junctions; however mediators of these signaling cascades are not fully understood. One such mediator, RhoC, is activated upon a number of external stimuli, such as epidermal growth factor (EGF), but its role as a mediator of EGF-stimulated migration and invasion has not been elucidated in HNSCC. In the present study, we investigate the role of RhoC as a mediator of EGF-stimulated migration and invasion in HNSCC. We show that upon EGF stimulation, EGFR and RhoC were strongly activated in HNSCC. This resulted in activation of the phosphatidylinositol 3-Kinase Akt pathway (PI3K-Akt), phosphorylation of GSK-3β at the Ser9 residue, and subsequent down regulation of E-cadherin cell surface expression resulting in increased tumor cell invasion. Knockdown of RhoC restored E-cadherin expression and inhibited EGF-stimulated migration and invasion. This is the first report in HNSCC demonstrating the role RhoC plays in mediating EGF-stimulated migration and invasion by down-regulating the PI3K-Akt pathway and E-cadherin expression. RhoC may serve as a treatment target for HNSCC.
机译：表皮生长因子受体（EGFR）在头部和颈部鳞状细胞癌（HNSCC）中过表达，其中已经显示出促进磷酸化上的肿瘤细胞侵袭。 EGFR促进肿瘤进展的一种机制是通过激活信号级联，从而导致E-Cadherin的丧失，细胞 - 细胞粘附结的跨膜糖蛋白;然而，这些信号传导级联的调解器不完全理解。在许多外部刺激（例如表皮生长因子（EGF））上激活一种这样的介质，rhoc，但其作为EGF刺激的迁移和侵袭的介质的作用尚未在HNSCC中阐明。在本研究中，我们调查RHOC作为HNSCC EGF刺激的迁移和侵袭的介质。我们表明，在EGF刺激时，在HNSCC中强烈激活EGFR和RHOC。这导致磷脂酰肌醇3-激酶AKT途径（PI3K-AKT），在SER9残余物中的GSK-3β的磷酸化，并随后对E-Cadherin细胞表面表达进行抑制导致肿瘤细胞侵袭增加。 rhoc的敲低恢复了e-cadherin表达并抑制EGF刺激的迁移和侵袭。这是HNSCC中的第一份报告，证明了在通过下调PI3K-AKT途径和E-Cadherin表达中介导EGF刺激的迁移和侵袭的角色rOC。 Rhoc可以作为HNSCC的治疗靶标。

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