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首页> 外文期刊>Frontiers in Public Health >Carbon Ion Irradiation Enhances the Anti-tumor Efficiency in Tongue Squamous Cell Carcinoma via Modulating the FAK Signaling
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Carbon Ion Irradiation Enhances the Anti-tumor Efficiency in Tongue Squamous Cell Carcinoma via Modulating the FAK Signaling

机译：通过调节FAK信号传导，碳离子辐射通过调节舌鳞状细胞癌中的抗肿瘤效率

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Oral cancer is a very aggressive disease with high rates of recurrence and metastasis. This study aimed at addressing how efficiently tongue cancer is suppressed after carbon ion irradiation. Here, the close relationship between upregulated expression of focal adhesion kinase (FAK) and high metastatic status in tongue squamous cell carcinoma patients was validated using bioinformatics and immunohistochemical analyses. Our data indicated that FAK suppression significantly enhanced the killing effect induced by irradiation in the tongue cancer cell line CAL27, as evidenced by increased apoptotic induction and reduced colony formation. More importantly, in FAK-deficient cells, carbon ion irradiation was shown to remarkably inhibit migration and invasion by delaying wound healing and slowing down motility. Further studies revealed that irradiation exposure caused disorganization of the actin cytoskeleton and reduced cell adhesive energy in FAK-deficient cells. Moreover, carbon ion treatment, in combination with FAK silencing, markedly blocked the phosphorylation levels of FAK, and paxillin, which partly contributed to the reduced motility of tongue squamous cell carcinoma CAL27 cells. Collectively, these results suggest that the prominent obstructing role of carbon ion irradiation in the growth inhibition and metastatic behavior of tumors, including attenuation of cell adhesiveness, motility, and invasiveness, could be distinctly modulated by FAK-mediated downstream pathways.
机译：口腔癌是一种非常侵略性的疾病，复发和转移率高。该研究旨在解决碳离子照射后有效抑制舌癌。这里，使用生物信息学和免疫组织化学分析验证了舌癌患者局灶性粘附激酶（FAK）和高转移状态的紧密关系。我们的数据表明，FAK抑制显着增强了舌癌细胞系CAL27中辐射诱导的杀伤效果，如凋亡诱导和降低的菌落形成所证明。更重要的是，在Fak缺陷的细胞中，显示碳离子辐射通过延迟伤口愈合和减缓动力来显着抑制迁移和侵袭。进一步的研究表明，照射暴露导致肌动蛋白细胞骨架的紊乱和在FAK缺陷细胞中减少细胞粘合能量。此外，碳离子处理与FAK沉默相结合，显着阻断了FAK和Paxillin的磷酸化水平，这部分导致了舌鳞状细胞癌CAL27细胞的活性降低。总的来说，这些结果表明碳离子照射在肿瘤生长抑制和转移行为中的突出阻塞作用，包括细胞粘合性，运动和侵袭性的衰减，可以通过FAK介导的下游途径明显地调节。

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