ArticleBiochemical genetics2024
Increased FGL1 Expression Predicts Poor Prognosis and Promotes EMT in Head and Neck Squamous Cell Carcinoma.
Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Hepatokine FGL1 drives endothelial injury and atherogenesisActa pharmaceutica Sinica. B · 2026Article
- Role of hepatocyte-derived fibrinogen-related protein 1 as a serum biomarker in the diagnosis of community-acquired pneumonia and sepsis: A cross-sectional study.The Journal of international medical research · 2026Observational
- Effect of fibrinogen like protein 1 on cisplatin-resistance in laryngeal carcinoma through targeting integrinβ1 in vivo and in vitro.Discover oncology · 2025Article
- Silencing FGL1 promotes prostate cancer cell apoptosis and inhibits EMT progression.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.