ArticleClinical cancer research : an official journal of the American Association for Cancer Research2015
Loss of SOD3 (EcSOD) Expression Promotes an Aggressive Phenotype in Human Pancreatic Ductal Adenocarcinoma.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
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- Evaluation of the efficacy and predictive indicators of PD- 1 inhibitors combined with chemotherapy in advanced pancreatic cancer.Scientific reports · 2025Article
- Single cell atlas reveals multilayered metabolic heterogeneity across tumour types.EBioMedicine · 2024Article
- Overexpression of Extracellular Superoxide Dismutase 3 Inhibits Cancer Cell Growth and Migration in Colorectal Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- Copper-Based Nanomedicines for Cuproptosis-Mediated Effective Cancer Treatment.Biomaterials research · 2024Review
- Cancer-associated fibroblast-related prognostic signature predicts prognosis and immunotherapy response in pancreatic adenocarcinoma based on single-cell and bulk RNA-sequencing.Scientific reports · 2023Article
- Cancer immune exclusion: breaking the barricade for a successful immunotherapy.Frontiers in oncology · 2023Review
- SOD3 Expression in Tumor Stroma Provides the Tumor Vessel Maturity in Oral Squamous Cell Carcinoma.Biomedicines · 2022Article
- Copper in the tumor microenvironment and tumor metastasis.Journal of clinical biochemistry and nutrition · 2022Article
- Targeting HIF-2α in the Tumor Microenvironment: Redefining the Role of HIF-2α for Solid Cancer Therapy.Cancers · 2022Review
- ROS-Related miRNAs Regulate Immune Response and Chemoradiotherapy Sensitivity in Hepatocellular Carcinoma by Comprehensive Analysis and Experiment.Oxidative medicine and cellular longevity · 2022Article
- Impact of EcSOD Perturbations in Cancer Progression.Antioxidants (Basel, Switzerland) · 2021Review
- ROS and TGFβ: from pancreatic tumour growth to metastasis.Journal of experimental & clinical cancer research : CR · 2021Review
- Association ofSOD3 promoter DNA methylation with its down-regulation in breast carcinomas.Epigenetics · 2020Article
- Review
- SOD3 induces a HIF-2α-dependent program in endothelial cells that provides a selective signal for tumor infiltration by T cells.Journal for immunotherapy of cancer · 2020Article
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
purposePancreatic ductal adenocarcinoma (PDA) cells are known to produce excessive amounts of reactive oxygen species (ROS), particularly superoxide, which may contribute to the aggressive and refractory nature of this disease. Extracellular superoxide dismutase (EcSOD) is an antioxidant enzyme that catalyzes the dismutation of superoxide in the extracellular environment. This study tests the hypothesis that EcSOD modulates PDA growth and invasion by modifying the redox balance in PDA. EXPERIMENTAL
designWe evaluated the prognostic significance of EcSOD in a human tissue microarray (TMA) of patients with PDA. EcSOD overexpression was performed in PDA cell lines and animal models of disease. The impact of EcSOD on PDA cell lines was evaluated with Matrigel invasion in combination with a superoxide-specific SOD mimic and a nitric oxide synthase (NOS) inhibitor to determine the mechanism of action of EcSOD in PDA.
resultsLoss of EcSOD expression is a common event in PDA, which correlated with worse disease biology. Overexpression of EcSOD in PDA cell lines resulted in decreased invasiveness that appeared to be related to reactions of superoxide with nitric oxide. Pancreatic cancer xenografts overexpressing EcSOD also demonstrated slower growth and peritoneal metastasis. Overexpression of EcSOD or treatment with a superoxide-specific SOD mimic caused significant decreases in PDA cell invasive capacity.
conclusionsThese results support the hypothesis that loss of EcSOD leads to increased reactions of superoxide with nitric oxide, which contributes to the invasive phenotype. These results allow for the speculation that superoxide dismutase mimetics might inhibit PDA progression in human clinical disease.
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