ArticleJournal of translational medicine2025
Nordihydroguaiaretic acid inhibits bladder cancer metastasis through suppression of α1,3-mannosyltransferase expression and LRFN4 N-glycosylation.
Article in Journal of translational medicine, 2025. 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
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Who cites it
2 citing papers in PubMed.
- Epigenetic regulation of NDGA and its synergistic inhibition with EZH2 inhibitors in prostate cancer via NRP1.Acta pharmacologica Sinica · 2026Article
- [Myricetin inhibits proliferation and migration of bladder cancer cells by inhibiting HSP90AA1-mediated AKT phosphorylation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetastasis remains a predominant contributor to cancer-related mortality worldwide. Elucidating the molecular mechanisms underlying cancer metastasis is crucial for developing strategies to inhibit tumor progression and improve clinical outcomes. Protein glycosylation, a hallmark of cancer pathogenesis mediated by specific glycosyltransferases, has emerged as a critical regulatory mechanism. This study investigates the functional role of glycosylation in cancer progression and explores its therapeutic potential.
methodsWe employed an integrated approach combining bioinformatics analysis of datasets, in vitro biological assays, transcriptional profiling, immunoprecipitation, and lectin pull-down assays to characterize α1,3-mannosyltransferase (ALG3)-dependent glycosylation mechanism in bladder cancer metastasis. Therapeutic targeting was investigated through virtual screening, molecular docking, molecular dynamics simulation, cellular thermal shift assay (CETSA), and validated in nude mice model using the Tranditional Chinese Medicine (TCM) monomer (NDGA).
resultsOur analysis revealed significantly elevated ALG3 expression in bladder cancer patients. Combined measurement of ALG3 in urine and serum samples demonstrated strong diagnostic potential, with higher AUC, sensitivity and specificity. Mechanistically, ALG3 promoted oncogenic cell behaviors through Ras signaling pathway activation. Immunoprecipitation and lectin pull-down assays identified LRFN4 as a novel ALG3 target, with ALG3 mediated N-glycosylation of LRFN4 being essential for its oncogenic function. Virtual screening identified nordihydroguaiaretic acid (NDGA) as a potent ALG3 inhibitor, which was validated through molecular docking, molecular dynamics simulation and CETSA. NDGA exhibited significant anti-tumor effects in both in vitro and in vivo models.
conclusionsOur findings established ALG3 as a promising detection glycobiomarker for bladder cancer, and a key regulator for metastasis through LRFN4 N-glycosylation and Ras signaling pathway activation. The identified ALG3 inhibitor-NDGA demonstrated significant therapeutic potential, offering a foundation for developing personalized treatment strategies against bladder cancer metastasis.
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