Translational cancer research · 2026
UBA6 serves as a prognostic biomarker and promotes tumor progression in pancreatic ductal adenocarcinoma.
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Xu Zesha, Zhang Yinghua, Wang Ying
Аннотация
BACKGROUND: The limited availability of reliable biomarkers for prognostic risk stratification in pancreatic ductal adenocarcinoma (PDAC) constrains long-term patient survival. There is a pressing need to identify molecular indicators possessing high sensitivity and specificity. This study aimed to evaluate the prognostic significance of UBA6 and its association with tumor progression in PDAC.
METHODS: Prognostic candidate genes were identified through univariate Cox regression analysis and subsequent Venn diagram intersection. Their expression profiles were contrasted across PDAC specimens and matched adjacent non-tumorous tissues in multiple independent cohorts. Cellular expression patterns were resolved using single-cell RNA sequencing data. The predictive accuracy for survival was evaluated via Kaplan-Meier (K-M) survival analysis, receiver operating characteristic (ROC) curves, and calibration plots. Associations between gene expression and immune cell infiltration levels were estimated using Pearson correlation. Functional pathway enrichment was investigated with Gene Set Enrichment Analysis (GSEA). The impact on malignant phenotypes was assessed through in vitro functional assays measuring proliferation [Cell Counting Kit-8 (CCK-8) and colony formation] and migration (Transwell).
RESULTS: Ubiquitin-like modifier activating enzyme 6 (UBA6) was robustly identified as a prognostic marker through Cox regression and intersection analysis. Its expression, both at the transcript and protein levels, was significantly upregulated in tumor tissues and associated with poorer patient outcomes. At the single‑cell resolution, UBA6 was found to be predominantly expressed in malignant ductal cells. Elevated UBA6 expression also correlated with reduced infiltration of CD8+ T cells. GSEA analysis inferred that high UBA6 expression was linked to pathways involved in ubiquitin‑mediated proteolysis, cell cycle, and p53 signaling. Correspondingly, functional assays confirmed that UBA6 knockdown suppressed the proliferative and migratory capacities of PDAC cells.
CONCLUSIONS: This study identifies UBA6 as a robust and independent predictor of overall survival (OS) in PDAC, validates its prognostic utility, and delineates its tumor-promoting role in disease progression. These findings enhance the understanding of PDAC pathogenesis and could inform the development of improved clinical management strategies.
METHODS: Prognostic candidate genes were identified through univariate Cox regression analysis and subsequent Venn diagram intersection. Their expression profiles were contrasted across PDAC specimens and matched adjacent non-tumorous tissues in multiple independent cohorts. Cellular expression patterns were resolved using single-cell RNA sequencing data. The predictive accuracy for survival was evaluated via Kaplan-Meier (K-M) survival analysis, receiver operating characteristic (ROC) curves, and calibration plots. Associations between gene expression and immune cell infiltration levels were estimated using Pearson correlation. Functional pathway enrichment was investigated with Gene Set Enrichment Analysis (GSEA). The impact on malignant phenotypes was assessed through in vitro functional assays measuring proliferation [Cell Counting Kit-8 (CCK-8) and colony formation] and migration (Transwell).
RESULTS: Ubiquitin-like modifier activating enzyme 6 (UBA6) was robustly identified as a prognostic marker through Cox regression and intersection analysis. Its expression, both at the transcript and protein levels, was significantly upregulated in tumor tissues and associated with poorer patient outcomes. At the single‑cell resolution, UBA6 was found to be predominantly expressed in malignant ductal cells. Elevated UBA6 expression also correlated with reduced infiltration of CD8+ T cells. GSEA analysis inferred that high UBA6 expression was linked to pathways involved in ubiquitin‑mediated proteolysis, cell cycle, and p53 signaling. Correspondingly, functional assays confirmed that UBA6 knockdown suppressed the proliferative and migratory capacities of PDAC cells.
CONCLUSIONS: This study identifies UBA6 as a robust and independent predictor of overall survival (OS) in PDAC, validates its prognostic utility, and delineates its tumor-promoting role in disease progression. These findings enhance the understanding of PDAC pathogenesis and could inform the development of improved clinical management strategies.