在CAF中FERMT2上调增强OSCC的EMT和M2巨细胞极化
Xiangrui Ma1,2, Dan Zhao3, Shan Liu4
1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Oral diseases
|June 26, 2023
概括
在口腔癌相关纤维细胞 (OCAFs) 中升级的FERMT2驱动口腔状细胞癌 (OSCC) 侵袭和M2巨分化,影响患者的生存.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 瘤微环境 瘤微环境
背景情况:
- FERMT2 (Filamin-2) 的上调与恶性行为有关,例如上皮细胞转化为介质细胞转化 (EMT).
- 口腔癌相关纤维细胞 (OCAFs) 在塑造瘤微环境方面发挥着至关重要的作用.
研究的目的:
- 在口腔状细胞癌 (OSCC) 中研究FERMT2表达.
- 探索FERMT2在OCAF介导的瘤微环境中的作用.
主要方法:
- 大量和单细胞RNA测序数据的生物信息分析 (TCGA-HNSC).
- 在体外研究中使用OSCC细胞系 (SCC15,CAL27),初级正常口腔纤维细胞 (NOF),OCAF和THP-1细胞.
主要成果:
- 在OCAF中,FERMT2的表达显著高于OSCC细胞和正常纤维细胞.
- 在OCAF中降低FERMT2降低了OSCC细胞入侵,介酶标记体表达和M0巨细胞向M2极化迁移.
- 在OSCC患者中,更高的FERMT2表达与不利的疾病特异性存活率 (DSS) 相相关.
结论:
- 在OCAF中的FERMT2促进OSCC EMT和M2巨细胞两极分化.
- FERMT2调节了IGFBP7,SPARC,COL4A1和IGFBP4等因素的OCAF分泌,影响了瘤的微环境.
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