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Apolipoprotein D downregulation in OSCC: multi-database validation and clinical significance
Shuting Wang1,2, Jun Zhao1,2, Rui Bai1,2
1Department of Oral and Maxillofacial Surgery, College & Hospital of Stomatology, Guangxi Medical University, No. 10 Shuangyong Road, Nanning, Guangxi, 530021, China.
BMC Medical Genomics
|March 11, 2026
Summary
Apolipoprotein D (APOD) is significantly reduced in oral squamous cell carcinoma (OSCC), showing potential as a diagnostic biomarker. Its downregulation may drive OSCC progression by disrupting the Type I interferon-JAK-STAT pathway.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Apolipoprotein D (APOD) is a lipocalin superfamily member involved in apoptosis, cancer, and neural repair.
- While APOD's role in various cancers is known, its significance in oral squamous cell carcinoma (OSCC) is understudied.
Purpose of the Study:
- To investigate the expression levels and clinical significance of APOD in OSCC.
- To explore the potential of APOD as a diagnostic and prognostic biomarker for OSCC.
Main Methods:
- Utilized multi-omics data from TCGA, GEO, and CPTAC databases for APOD mRNA and protein analysis.
- Validated findings using qRT-PCR and immunohistochemistry on OSCC tissue samples.
- Assessed diagnostic and prognostic potential via sROC curves, Kaplan-Meier analysis, and multivariate Cox regression; explored pathways using GSEA.
Main Results:
- APOD mRNA and protein were significantly downregulated in OSCC tissues compared to normal controls, confirmed in clinical samples.
- APOD showed potential as a diagnostic biomarker for OSCC; pathological T stage was an independent prognostic factor.
- GSEA revealed APOD positively correlates with Type I interferon signaling, suggesting its downregulation inhibits this pathway, potentially promoting OSCC progression.
Conclusions:
- APOD expression is markedly reduced in OSCC, indicating its potential as a diagnostic and prognostic biomarker.
- Downregulation of APOD may contribute to OSCC progression by impairing the Type I interferon-mediated JAK-STAT signaling pathway.
Keywords:
Apolipoprotein DBioinformaticsClinical significanceOral squamous cell carcinomaType I interferon-JAK-STATMore Related Videos
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