ArticleInternational journal of biological sciences2026
CXCL8 Drives MMP1 Upregulation and Promotes Metastatic Progression in Oral Cancer Through CXCR1/2-Mediated JAK1/STAT3 Activation.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Dexmedetomidine alleviates acute lung injury in humans by modulating the JAK1-STAT3 axis.Experimental and therapeutic medicine · 2026Article
- Identification of Inflammatory Markers for the Prediction and Diagnosis of Diminished Ovarian Reserve Using Olink Targeted Proteomics.Journal of clinical medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Oral squamous cell carcinoma (OSCC) is an aggressive malignancy, frequently diagnosed at advanced stages with regional and distant metastases that compromise survival. Identifying key molecular regulators of OSCC progression is essential for developing targeted therapies. Although CXCL8 is elevated in OSCC and linked to tumor progression, its precise pro-metastatic mechanisms and downstream effectors remain unclear. Methods: To identify key regulators of OSCC metastasis, we integrated bioinformatics analysis of multiple GEO datasets and identified CXCL8 as an upregulated hub gene in OSCC tissues. Functional assays were performed in OSCC cell lines (SCC4, SCC9, HSC3) to investigate the role of CXCL8 in cell migration and elucidate its downstream signaling pathways. An orthotopic tongue xenograft mouse model was established to validate the Results: CXCL8 expression was significantly upregulated in OSCC tissues and strongly correlated with enhanced cell motility in OSCC cell lines. High CXCL8 expression was associated with poor overall survival in head and neck cancer patients. Mechanistically, CXCL8 upregulated matrix metalloproteinase 1 (MMP1) expression and enhanced cell migration through activation of the CXCR1/2-JAK1-STAT3 signaling axis. CXCL8 treatment induced JAK1 and STAT3 phosphorylation, promoted STAT3 nuclear translocation, and directly activated MMP1 promoter activity. Pharmacological inhibition or siRNA-mediated silencing of CXCR1/2, JAK1, STAT3, or MMP1 significantly reversed CXCL8-induced cell migration, wound healing, and MMP1 expression. Conclusion: This study reveals that CXCL8 drives OSCC metastasis via CXCR1/2-mediated JAK1/STAT3 activation leading to MMP1 transcriptional upregulation. Our findings establish CXCL8 as both a prognostic biomarker and a promising therapeutic target, and suggest that targeting this pathway offers significant therapeutic potential for preventing OSCC metastatic progression.
Indexed as
Identifiers
What OpenQuestion holds
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.