FGF8 诱导口腔鳞状细胞癌上皮-间充质转化并促进转移。
FGF8 induces epithelial-mesenchymal transition and promotes metastasis in oral squamous cell carcinoma.
机构信息
The Affiliated Hospital of Stomatology, School of Stomatology, Zhejiang University School of Medicine and Key Laboratory of Oral Biomedical Research of Zhejiang Province, Hangzhou, China.
State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management & West China Hospital of Stomatology, Sichuan University, Chengdu, China.
出版信息
Int J Oral Sci. 2021 Mar 1;13(1):6. doi: 10.1038/s41368-021-00111-x.
Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide, and with 354 864 new cases each year. Cancer metastasis, recurrence, and drug resistance are the main causes to cripples and deaths of OSCC patients. As potent growth factors, fibroblast growth factors (FGFs) are frequently susceptible to being hijacked by cancer cells. In this study, we show that FGF8 is upregulated in OSCC tissues and high FGF8 expression is related with a set of clinicopathologic parameters, including age, drinking, and survival time. FGF8 treatment enhances the invasive capability of OSCC cells. Lentivirus-based FGF8 expression promotes OSCC metastasis in a mouse lung metastasis model. Further, mechanistic study demonstrates that FGF8 induces epithelial-mesenchymal transition (EMT) in OSCC cells. These results highlight a pro-metastatic function of FGF8, and underscore the role of FGF8 in OSCC development.
口腔鳞状细胞癌（OSCC）是全球最常见的癌症之一，每年有 354864 例新发病例。癌症转移、复发和耐药性是导致 OSCC 患者致残和死亡的主要原因。成纤维细胞生长因子（FGFs）作为有效的生长因子，经常容易被癌细胞劫持。在本研究中，我们发现 FGF8 在 OSCC 组织中上调，高 FGF8 表达与一系列临床病理参数相关，包括年龄、饮酒和生存时间。FGF8 处理可增强 OSCC 细胞的侵袭能力。基于慢病毒的 FGF8 表达促进了 OSCC 细胞在小鼠肺转移模型中的转移。此外，机制研究表明 FGF8 可诱导 OSCC 细胞发生上皮-间充质转化（EMT）。这些结果突出了 FGF8 的促转移功能，并强调了 FGF8 在 OSCC 发展中的作用。
Zotero 插件