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FGL1表达增加预示头颈部鳞状细胞癌预后不良并促进上皮-间质转化

Increased FGL1 Expression Predicts Poor Prognosis and Promotes EMT in Head and Neck Squamous Cell Carcinoma.

作者信息

Pan Zhiyong, Hu Weiqun, Huang Jinqiao, Zheng Zhicong, Lin Enrun, Wang PingPing, Mao Linwei

机构信息

Department of Otolaryngology, Affiliated Hospital of Putian University, Putian, Fujian, PR China.

Department of Pathology, Affiliated Hospital of Putian University, Putian, Fujian, PR China.

出版信息

Biochem Genet. 2024 Jun;62(3):2066-2081. doi: 10.1007/s10528-023-10545-z. Epub 2023 Oct 16.

Abstract

Fibrinogen-like protein 1 (FGL1) is a proliferation- and metabolism-related factor secreted by the liver that is aberrantly expressed and functionally abnormal in human malignancies. However, the role of FGL1 in head and neck squamous cell carcinoma (HNSCC) remains unknown. We analysed FGL1 expression in HNSCC and its impact on patient survival using the TCGA database. The role of FGL1 in HNSCC cells was investigated by Cell Counting Kit-8, colony formation, and Transwell assays. In addition, we conducted in vivo experiments to assess the effect of FGL1 knockdown on tumour growth. We found that FGL1 was highly expressed in HNSCC and correlated with a poor prognosis. Downregulation of FGL1 expression inhibited the proliferation and invasion of HNSCC cells. Furthermore, mechanistic analysis revealed that FGL1 induced an epithelial-mesenchymal transition (EMT) phenotype and, thus, the malignant progression of HNSCC cells. Finally, xenograft models showed that FGL1 knockdown significantly inhibited EMT in HNSCC in vivo. Our study revealed that FGL1, an oncogene, promotes the malignant progression of HNSCC, providing new perspective on and potential therapeutic target for the treatment of HNSCC.

摘要

纤维蛋白原样蛋白1(FGL1)是一种由肝脏分泌的与增殖和代谢相关的因子,在人类恶性肿瘤中表达异常且功能异常。然而,FGL1在头颈部鳞状细胞癌(HNSCC)中的作用仍不清楚。我们使用TCGA数据库分析了FGL1在HNSCC中的表达及其对患者生存的影响。通过细胞计数试剂盒-8、集落形成和Transwell实验研究了FGL1在HNSCC细胞中的作用。此外,我们进行了体内实验,以评估FGL1基因敲低对肿瘤生长的影响。我们发现FGL1在HNSCC中高表达,且与预后不良相关。FGL1表达下调抑制了HNSCC细胞的增殖和侵袭。此外,机制分析表明,FGL1诱导上皮-间质转化(EMT)表型,从而促进HNSCC细胞的恶性进展。最后,异种移植模型表明,FGL1基因敲低在体内显著抑制了HNSCC中的EMT。我们的研究表明,癌基因FGL1促进了HNSCC的恶性进展,为HNSCC的治疗提供了新的视角和潜在的治疗靶点。

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