SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2

BackgroundPancreatic ductal adenocarcinoma (PDAC) is highly malignant with a poor prognosis, posing significant clinical challenges. SUMOylation, a reversible post-translational modification, plays a critical role in tumor progression, yet its prognostic significance in PDAC remains unclear.MethodsW...

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Main Authors: Xiangjun Wang, Chuanxin Yang, Yangming Liu, Jian Wang
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-04-01
Series:Frontiers in Pharmacology
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Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2025.1532658/full
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author Xiangjun Wang
Chuanxin Yang
Yangming Liu
Jian Wang
author_facet Xiangjun Wang
Chuanxin Yang
Yangming Liu
Jian Wang
author_sort Xiangjun Wang
collection DOAJ
description BackgroundPancreatic ductal adenocarcinoma (PDAC) is highly malignant with a poor prognosis, posing significant clinical challenges. SUMOylation, a reversible post-translational modification, plays a critical role in tumor progression, yet its prognostic significance in PDAC remains unclear.MethodsWe assessed SUMOylation expression patterns and function in PDAC using Western blot and the SUMOylation inhibitor TAK-981. Differentially expressed SUMOylation substrate encoding genes (DE-SSEGs) were identified from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression Project (GTEx) datasets. A SUMOylation-based prognostic model, Sscore, was constructed using LASSO and Cox regression. Additional analyses included somatic mutation, immune infiltration, TIDE, drug sensitivity, and single-cell RNA sequencing. The role of SAFB2 in PDAC was validated in vitro.ResultsPDAC cells showed elevated SUMOylation, and its inhibition reduced cell proliferation. The Sscore model, based on DE-SSEGs (CDK1, AHNAK2, SAFB2), predicted overall survival and correlated with genome variation, immune infiltration, and drug sensitivity. Single-cell analysis further confirmed a link between high Sscore and malignancy. SAFB2, identified as a pivotal gene within the Sscore model, was significantly downregulated in PDAC tissues and cell lines; its overexpression was shown to inhibit PDAC cell proliferation, migration, and invasion by suppressing the Wnt/β-Catenin signaling pathway.ConclusionThis study underscores the role of SUMOylation in PDAC and introduces the Sscore as a prognostic tool. SAFB2 is identified as a potential tumor suppressor, offering new therapeutic targets for PDAC.
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spelling doaj-art-6b412de9d7584df2b5248db205d3ad5e2025-08-20T02:26:24ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-04-011610.3389/fphar.2025.15326581532658SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2Xiangjun WangChuanxin YangYangming LiuJian WangBackgroundPancreatic ductal adenocarcinoma (PDAC) is highly malignant with a poor prognosis, posing significant clinical challenges. SUMOylation, a reversible post-translational modification, plays a critical role in tumor progression, yet its prognostic significance in PDAC remains unclear.MethodsWe assessed SUMOylation expression patterns and function in PDAC using Western blot and the SUMOylation inhibitor TAK-981. Differentially expressed SUMOylation substrate encoding genes (DE-SSEGs) were identified from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression Project (GTEx) datasets. A SUMOylation-based prognostic model, Sscore, was constructed using LASSO and Cox regression. Additional analyses included somatic mutation, immune infiltration, TIDE, drug sensitivity, and single-cell RNA sequencing. The role of SAFB2 in PDAC was validated in vitro.ResultsPDAC cells showed elevated SUMOylation, and its inhibition reduced cell proliferation. The Sscore model, based on DE-SSEGs (CDK1, AHNAK2, SAFB2), predicted overall survival and correlated with genome variation, immune infiltration, and drug sensitivity. Single-cell analysis further confirmed a link between high Sscore and malignancy. SAFB2, identified as a pivotal gene within the Sscore model, was significantly downregulated in PDAC tissues and cell lines; its overexpression was shown to inhibit PDAC cell proliferation, migration, and invasion by suppressing the Wnt/β-Catenin signaling pathway.ConclusionThis study underscores the role of SUMOylation in PDAC and introduces the Sscore as a prognostic tool. SAFB2 is identified as a potential tumor suppressor, offering new therapeutic targets for PDAC.https://www.frontiersin.org/articles/10.3389/fphar.2025.1532658/fullPancreatic ductal adenocarcinomaSUMOylationTAK-981PrognosisSAFB2Wnt/β-Catenin signaling pathway
spellingShingle Xiangjun Wang
Chuanxin Yang
Yangming Liu
Jian Wang
SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2
Frontiers in Pharmacology
Pancreatic ductal adenocarcinoma
SUMOylation
TAK-981
Prognosis
SAFB2
Wnt/β-Catenin signaling pathway
title SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2
title_full SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2
title_fullStr SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2
title_full_unstemmed SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2
title_short SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of SAF-B2
title_sort sumoylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment of saf b2
topic Pancreatic ductal adenocarcinoma
SUMOylation
TAK-981
Prognosis
SAFB2
Wnt/β-Catenin signaling pathway
url https://www.frontiersin.org/articles/10.3389/fphar.2025.1532658/full
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