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癌细胞和巨细胞之间的交叉声会通过CXCL1/EGF正反循环促进OSCC细胞的迁移和入侵
Wei Huang1, Mingjing Jiang1, Ying Lin1
1Experimental Teaching Center, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, 110001, China.
口腔状细胞癌 (OSCC) 细胞分泌C-X-C动机化学因子连接体1 (CXCL1),刺激巨细胞产生上皮生长因子 (EGF). 然后,这个EGF促进OSCC细胞的入侵和迁移,形成一个反循环,推动癌症的进展.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 口腔状细胞癌 (OSCC) 细胞和瘤相关的巨细胞表现出复杂的相互作用.
- 在这种交叉中,C-X-C动机化学基因配体1 (CXCL1) 和上皮生长因子 (EGF) 是关键的分泌因子.
- 控制OSCC细胞-巨细胞通信的精确机制在很大程度上是未知的.
研究的目的:
- 阐明OSCC细胞和巨细胞之间的交叉对话背后的分子机制.
- 研究CXCL1和EGF在OSCC进展中的作用.
- 确定OSCC的潜在治疗点.
主要方法:
- 免疫组织化学,RT-PCR和ELISA用于检测OSCC样本和细胞系中的CXCL1和EGF表达.
- 进行细胞增殖,迁移和入侵分析 (CCK-8,殖民地形成,伤口愈合,Transwell) 以评估EGF对OSCC细胞的影响.
- 西方涂抹,RT-PCR和免疫光被用来分析上皮质-介质细胞过渡 (EMT) 和信号通路 (NF-κB).
- 使用RT-PCR和流细胞计,评估了巨细胞的两极分化.
主要成果:
- 与正常角质细胞相比,OSCC细胞 (Cal27) 表达的CXCL1水平较高.
- 在巨细胞中,OSCC衍生的CXCL1上调了EGF的表达.
- EGF刺激促进了OSCC细胞的增殖,迁移,入侵和EMT.
- EGF诱导的OSCC细胞入侵和迁移是由通过EGFR激活NF-κB信号传递的.
- 在EGF增强OSCC细胞的CXCL1产生时,确定了一个积极的反循环.
结论:
- 由OSCC细胞衍生的CXCL1刺激M2巨细胞的两极分化和EGF分泌.
- 通过NF-κB信号激活,EGF促进OSCC细胞的迁移和入侵.
- 在OSCC细胞和巨细胞之间的相互反循环有助于OSCC的进展.
- 针对CXCL1-EGF-NF-κB轴可能为OSCC提供治疗策略.
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