ArticleHeliyon2023
Identification of ALG3 as a potential prognostic biomarker in lung adenocarcinoma.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Post-translational modification signature shapes the tumor immune microenvironment and predicts clinical outcomes in melanoma.Discover oncology · 2026Article
- Inhibition of α-1,3-mannosyltransferase sensitizes head and neck squamous cell carcinomas to cetuximab via endoplasmic reticulum stress.Cell stress & chaperones · 2026Article
- Identification and validation of parthanatos-related genes in lung adenocarcinoma and construction of a prognostic risk model.Frontiers in immunology · 2026Article
- ALG3 as a PanCancer Oncogene: Bioinformatics Analysis and Identification of Small-Molecule Inhibitors.Anti-cancer agents in medicinal chemistry · 2026Article
- Nordihydroguaiaretic acid inhibits bladder cancer metastasis through suppression of α1,3-mannosyltransferase expression and LRFN4 N-glycosylation.Journal of translational medicine · 2025Article
- [Construction and Validation of A Prognostic Model for Lung Adenocarcinoma Based on Ferroptosis-related Genes].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
- Predicting prognosis in lung adenocarcinoma by predicting TIGIT expression: a pathomics model.Journal of thoracic disease · 2024Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The abnormal expression of Alpha-1,3-mannosyltransferase (ALG3) has been implicated in tumor promotion. However, the clinical significance of ALG3 in Lung Adenocarcinoma (LUAD) remains poorly understood. Therefore, we aimed to assess the prognostic value of ALG3 and its association with immune infiltrates in LUAD. Methods: The transcriptional expression profiles of ALG3 were obtained from the Cancer Genome Atlas (TCGA), comparing lung adenocarcinoma tissue with normal tissues. To determine the prognostic significance of AGL3, Kaplan-Meier plotter, and Cox regression analysis were employed. Logistic regression was utilized to analyze the association between ALG3 expression and clinical characteristics. Additionally, a receiver operating characteristic (ROC) curve and a nomogram were constructed. To explore the underlying mechanisms, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and gene set enrichment analysis (GSEA) was conducted. The relationship between AGL3A mRNA expression and immune infiltrates was investigated using the tumor immune estimation resource (TIMER) and tumor-immune system interaction database (TISIDB). Furthermore, an in vitro experiment was performed to assess the impact of ALG3 mRNA on lung cancer stemness abilities and examine key signaling pathway proteins. Results: Our results revealed the ALG3 mRNA and protein expression in patients with LUAD was much higher than that in adjacent normal tissues. High expression of ALG3 was significantly associated with N stage (N0, HR = 1.98, P = 0.002), pathological stage (stage I, HR = 2.09, P = 0.003), and the number of pack years (<40, HR = 2.58, P = 0.001). Kaplan-Meier survival analysis showed that high expression of ALG3 was associated with poor overall survival (P < 0.001), disease-free survival (P < 0.001), and progression-free interval (P = 0.007). Through multivariate analysis, it was determined that elevated ALG3 expression independently impacted overall survival (HR = 1.325, P = 0.04). The Tumor Immune Estimation Resource discovered a link between ALG3 expression and tumor-infiltrating immune cells in LUAD. Additionally, ROC analysis proved that ALG3 is a reliable diagnostic marker for LUAD (AUC:0.923). Functional pathways analysis identified that ALG3 is negatively correlated with FAT4. We performed qRT-PCR to assess that knockdown ALG3 expression significantly upregulated FAT4 expression. Spheroid assay and flow cytometry analysis results showed that downregulated of ALG3 inhibited H1975 cell line stemness. Western blot analysis revealed that decreased ALG3 inhibited the YAP/TAZ signal pathway. Conclusion: High expression of ALG3 is strongly associated with poor prognosis and immune infiltrates in LUAD.
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