ArticleOncology letters2025
Proteomics reveals the regulation of ALG1 expression by lentivirus-mediated THBS1 overexpression and its mechanism in meibomian gland carcinoma.
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Correlation between ocular tumor distribution and age based on analysis of pathological specimens.American journal of translational research · 2026Article
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7 authors.
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Abstract
Meibomian gland carcinoma (MGC) is a highly aggressive eyelid malignancy with a poor prognosis. MicroRNA-3907 (miR-3907) is upregulated in MGC, where it promotes tumor progression by suppressing thrombospondin 1 (THBS1). The present study aimed to assess the downstream regulatory mechanisms of THBS1 in MGC. Utilizing 4D label-free quantitative proteomics, chitobiosyldiphosphodolichol β-mannosyltransferase 1 (ALG1) was identified as the most significantly differentially expressed downstream protein following lentivirus-mediated overexpression of THBS1, with results corroborated by consistent sequencing data. Protein-protein docking models predicted a stable interaction between THBS1 and ALG1, mediated by hydrogen bonds involving key amino acid residues such as ASN-991 and MET-58. Co-immunoprecipitation and immunofluorescence assays confirmed the physical interaction and co-localization of THBS1 and ALG1 in MGC cells. Notably, ALG1 mRNA levels were significantly elevated in MGC cells compared with in normal meibomian gland cells. Functional assays revealed that ALG1 knockdown markedly suppressed malignant cellular behaviors and modulated the expression of genes associated with epithelial-mesenchymal transition, a key process in tumor metastasis. Conversely, ALG1 overexpression enhanced these malignant traits. Together, these findings highlight ALG1 as a critical downstream effector in the miR-3907/THBS1/ALG1 regulatory axis and suggest its potential as a biomarker for targeted diagnosis and therapy in MGC. The present study provides new insights into the molecular mechanisms underlying MGC and offers a basis for developing personalized therapeutic strategies.
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