SERPINB5 promotes pancreatic adenocarcinoma progression through FBXO32-mediated regulation of epithelial-mesenchymal transition

A study reported in Molecular Biology Reports found that silencing SERPINB5 reduced pancreatic adenocarcinoma cell proliferation, colony formation, migration and invasion, while changes in epithelial–mesenchymal transition-related proteins were reversed by restoring FBXO32 expression. The authors concluded that the SERPINB5/FBXO32 axis may contribute to pancreatic adenocarcinoma progression through regulation of epithelial–mesenchymal transition, although their findings come primarily from transcriptomic analyses and laboratory cell models.

The investigators screened differentially expressed genes in the TCGA-PAAD, GSE32676 and GSE101448 datasets. They used LASSO Cox regression and receiver operating characteristic curve analysis to identify prognostic candidates, selecting SERPINB5 for further investigation. Expression was examined in pancreatic adenocarcinoma cell lines, and the effects of SERPINB5 silencing were assessed with CCK-8 and colony-formation assays, Transwell migration and invasion assays, immunofluorescence, and Western blotting. Co-immunoprecipitation and rescue experiments were used to examine the relationship between SERPINB5 and FBXO32.

According to the abstract, a seven-gene risk model included SERPINB5 among its candidate prognostic genes. Single-gene ROC analyses distinguished pancreatic adenocarcinoma tumors from normal pancreatic tissues in all three transcriptomic datasets, with reported areas under the curve of 0.851, 0.966 and 0.965. SERPINB5 expression was consistently high in pancreatic adenocarcinoma tissues and cell lines. In the cell experiments, SERPINB5 knockdown inhibited proliferation, colony formation, migration and invasion. It also increased E-cadherin expression while reducing Vimentin and N-cadherin levels. Co-immunoprecipitation indicated a physical interaction between SERPINB5 and FBXO32, and SERPINB5 knockdown reduced FBXO32 expression.

The rescue experiments provide the central mechanistic result reported in the abstract: FBXO32 overexpression reversed the malignant cellular phenotypes and epithelial–mesenchymal transition-related changes produced by SERPINB5 silencing. This supports the authors’ interpretation that FBXO32 acts downstream of, or functionally compensates for, SERPINB5 in the studied cell models. The findings identify SERPINB5 as a candidate diagnostic and prognostic marker, but the evidence presented does not establish clinical performance or patient benefit. The available source is an abstract and article preview rather than the full report, and the experimental results are based on pancreatic adenocarcinoma cell lines rather than a prospective clinical cohort or patient outcomes.

Subject of Research: SERPINB5 and FBXO32 regulation of epithelial–mesenchymal transition in pancreatic adenocarcinoma cell models

Article Title: SERPINB5 promotes pancreatic adenocarcinoma progression through FBXO32-mediated regulation of epithelial-mesenchymal transition

Article References: Jiang, H., Zhang, P.-J., Li, W., & Zhang, H.-F. (2026). SERPINB5 promotes pancreatic adenocarcinoma progression through FBXO32-mediated regulation of epithelial-mesenchymal transition. Molecular Biology Reports, 53(1), Article 1719. https://doi.org/10.1007/s11033-026-12945-x

Image Credits: AI Generated

DOI: 10.1007/s11033-026-12945-x

Keywords: pancreatic adenocarcinoma, SERPINB5, FBXO32, epithelial–mesenchymal transition, cell proliferation, cell migration, cell invasion, transcriptomics, prognostic biomarkers, promotes, pancreatic, adenocarcinoma