补充成分C1r和C1s促进口腔状细胞癌细胞的增殖
Thinh Thi Kim Truong1, Tatsufumi Fujimoto2, Shinsuke Fujii3
1Laboratory of Oral Pathology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Journal of oral biosciences
|November 22, 2025
概括
补体系统,特别是C1r/C1s,通过激活ERK/AKT信号,促进口腔状细胞癌 (OSCC) 的生长. 这表明在OSCC发育过程中,无论表皮的起源如何,都有一个共同的机制.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 口腔状细胞癌 (OSCC) 是最常见的口腔癌,起源于粘膜或牙上皮质.
- 基因表达分析显示,在OSCC病变中",补充"基因组的增加.
- 补充系统在OSCC瘤发生中的作用尚不清楚.
研究的目的:
- 调查补充成分在口腔状细胞癌 (OSCC) 的发展中的参与.
- 探索补充系统激活和OSCC细胞增殖和信号通路之间的关系.
主要方法:
- 利用siRNA和shRNA在体外和体内评估OSCC细胞增殖.
- 采用西方涂抹来分析细胞内信号通路的激活.
- 通过免疫组织化学研究OSCC组织中的C1s表达,并评估MEK1/2抑制的影响.
主要成果:
- C1r/C1s表达正调节了ERK和AKT激活,促进了OSCC细胞的生长.
- 在激活ERK控制C1r/C1s表达的地方发现了负反循环.
- 在OSCC瘤中高C1s表达与高酸化ERK和Ki-67水平相关.
结论:
- 补体系统,特别是C1r/C1s,似乎是来自不同表皮原点的OSCC瘤发生的常见分子机制.
- 增加的C1r/C1s表达显著促进了口腔状细胞癌细胞的增殖.
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