ArticleCells2026
SOX11 Is Regulated by EGFR-STAT3 and Promotes Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor SOX11 is implicated in tumor progression across multiple types of cancers, including head and neck squamous cell carcinoma (HNSCC). However, its mechanistic role in HNSCC remains elusive. In this study, we found that the expression of SOX11 was induced by epidermal growth factor (EGF) but suppressed by an epidermal growth factor receptor (EGFR) inhibitor in HNSCC cells. The signal transducer and activator of transcription 3 (STAT3) bound to the Sox11 gene promoter and transcriptionally upregulated the expression of Sox11 in HNSCC cells. Meanwhile, analyses of The Cancer Genome Atlas (TCGA) gene expression datasets indicated that Sox11 gene expression was significantly overexpressed in HNSCC versus adjacent normal tissues and correlated with those of most epithelial-mesenchymal transition transcription factors (EMT-TFs) and marker genes. Knockdown of SOX11 significantly downregulated the expression of EMT-related genes, including EMT-TFs, vimentin, fibronectin, and N-cadherin, but significantly upregulated E-cadherin and vice versa when SOX11 was overexpressed. Collectively, our studies demonstrated that SOX11 was regulated by EGF-EGFR-STAT3 signals, promoting EMT in 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 Socratic graph.