ArticleMolecular cancer research : MCR2012
Genetic and epigenetic inactivation of extracellular superoxide dismutase promotes an invasive phenotype in human lung cancer by disrupting ECM homeostasis.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 82 citations in OpenAlex.
- Multifaceted roles of superoxide dismutases (SODs) in cellular homeostasis and cancer progression: Redox regulation and therapeutic implications.Journal of medical biochemistry · 2026Article
- Biomimetic FeCurrent pharmaceutical biotechnology · 2026Article
- Targeting Oxidative and Nitrosative Stress: Mechanistic Insights and Therapeutic Strategies for Radiation-Induced Lung Injury.Journal of inflammation research · 2026Review
- Oncotransformation in Bhas 42 Cell Transformation Assay by Typical Non-Genotoxic Carcinogens, PFOA and PFOS, and Time-Course Transcriptome Analysis.Biomolecules · 2025Article
- Redox Balance in Cancer in the Context of Tumor Prevention and Treatment.Biomedicines · 2025Review
- 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
- Review
- 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
- Urinary protein biomarker panel predicts esophageal squamous carcinoma from control cases and other tumors.Esophagus : official journal of the Japan Esophageal Society · 2022Article
- Copper in the tumor microenvironment and tumor metastasis.Journal of clinical biochemistry and nutrition · 2022Article
- Adenylate Kinase Isozyme 3 Regulates Mitochondrial Energy Metabolism and Knockout Alters HeLa Cell Metabolism.International journal of molecular sciences · 2022Article
- Targeting HIF-2α in the Tumor Microenvironment: Redefining the Role of HIF-2α for Solid Cancer Therapy.Cancers · 2022Review
- Green Nanoarchitectonics of Silver Nanoparticles for Antimicrobial Activity Against Resistant Pathogens.Journal of inorganic and organometallic polymers and materials · 2022Article
- Impact of EcSOD Perturbations in Cancer Progression.Antioxidants (Basel, Switzerland) · 2021Review
- High serum superoxide dismutase activity improves radiation-related quality of life in patients with esophageal squamous cell carcinoma.Clinics (Sao Paulo, Brazil) · 2021Article
- Interplay between Mitochondrial Metabolism and Cellular Redox State Dictates Cancer Cell Survival.Oxidative medicine and cellular longevity · 2021Review
- The Involvement of the Oxidative Stress Status in Cancer Pathology: A Double View on the Role of the Antioxidants.Oxidative medicine and cellular longevity · 2021Review
- Palladium Nanoparticle-Induced Oxidative Stress, Endoplasmic Reticulum Stress, Apoptosis, and Immunomodulation Enhance the Biogenesis and Release of Exosome in Human Leukemia Monocytic Cells (THP-1).International journal of nanomedicine · 2021Article
- Association ofSOD3 promoter DNA methylation with its down-regulation in breast carcinomas.Epigenetics · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular superoxide dismutase (EcSOD) is an important superoxide scavenger in the lung in which its loss, sequence variation, or abnormal expression contributes to lung diseases; however, the role of EcSOD in lung cancer has yet to be studied. We hypothesized that EcSOD loss could affect malignant progression in lung, and could be either genetic or epigenetic in nature. To test this, we analyzed EcSOD expression, gene copy number, promoter methylation, and chromatin accessibility in normal lung and carcinoma cells. We found that normal airway epithelial cells expressed abundant EcSOD and had an unmethylated promoter, whereas EcSOD-negative lung cancer cells displayed aberrant promoter hypermethylation and decreased chromatin accessibility. 5-aza-dC induced EcSOD suggesting that cytosine methylation was causal, in part, to silencing. In 48/50 lung tumors, EcSOD mRNA was significantly lower as early as stage I, and the EcSOD promoter was hypermethylated in 8/10 (80%) adenocarcinomas compared with 0/5 normal lung samples. In addition, 20% of the tumors showed loss of heterozygosity (LOH) of EcSOD. Reexpression of EcSOD attenuated the malignant phenotype of lung carcinoma cells by significantly decreasing invasion and survival. Finally, EcSOD decreased heparanase and syndecan-1 mRNAs in part by reducing NF-κB. By contrast, MnSOD and CuZnSOD showed no significant changes in lung tumors and had no effect on heparanase expression. Taken together, the loss of EcSOD expression is unique among the superoxide dismutases in lung cancer and is the result of EcSOD promoter methylation and LOH, suggesting that its early loss may contribute to ECM remodeling and malignant progression.
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