ArticlePloS one2013
Deletion of glutathione peroxidase-2 inhibits azoxymethane-induced colon cancer development.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- The Role of Se-Containing Glutathione Peroxidases and Thioredoxin Reductases in Oncogenesis: Expression Paradoxes and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Selenium: A Key Element in Inflammatory Bowel Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Evaluation of the Use of Cell Lines in Studies of Selenium-Dependent Glutathione Peroxidase 2 (GPX2) Involvement in Colorectal Cancer.Diseases (Basel, Switzerland) · 2024Article
- SELENOP modifies sporadic colorectal carcinogenesis and WNT signaling activity through LRP5/6 interactions.The Journal of clinical investigation · 2023Article
- The selenoprotein P-LRP5/6-WNT3A complex promotes tumorigenesis in sporadic colorectal cancer.The Journal of clinical investigation · 2023Article
- Clinicopathological characteristics, molecular features and novel diagnostic strategies for the detection of malignant transformation of endometriosis (Review).Experimental and therapeutic medicine · 2023Review
- Oxidative Stress, Inflammation and Colorectal Cancer: An Overview.Antioxidants (Basel, Switzerland) · 2023Review
- Antioxidant and Anti-Tumor Effects of Dietary Vitamins A, C, and E.Antioxidants (Basel, Switzerland) · 2023Review
- Revisiting therapeutic strategies for ovarian cancer by focusing on redox homeostasis.Oncology letters · 2022Review
- Prediction of Pathogenic Factors in Dysbiotic Gut Microbiomes of Colorectal Cancer Patients Using Reverse Microbiomics.Frontiers in oncology · 2022Article
- Comprehensive Review of Methodology to Detect Reactive Oxygen Species (ROS) in Mammalian Species and Establish Its Relationship with Antioxidants and Cancer.Antioxidants (Basel, Switzerland) · 2021Review
- Antioxidant Gene Signature Impacts the Immune Infiltration and Predicts the Prognosis of Kidney Renal Clear Cell Carcinoma.Frontiers in genetics · 2021Article
- Distinct and overlapping functions of glutathione peroxidases 1 and 2 in limiting NF-κB-driven inflammation through redox-active mechanisms.Redox biology · 2020Article
- Selenium and selenoproteins in prostanoid metabolism and immunity.Critical reviews in biochemistry and molecular biology · 2019Review
- Selenium, Selenoproteins and Viral Infection.Nutrients · 2019Review
- Selenoproteins in colon cancer.Free radical biology & medicine · 2018Review
- Roles for selenium and selenoprotein P in the development, progression, and prevention of intestinal disease.Free radical biology & medicine · 2018Review
- Loss of epithelium-specific GPx2 results in aberrant cell fate decisions during intestinal differentiation.Oncotarget · 2018Article
- Selenoproteins in Tumorigenesis and Cancer Progression.Advances in cancer research · 2017Review
- Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications.Physiological reviews · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The selenoprotein glutathione peroxidase-2 (GPx2) appears to have a dual role in carcinogenesis. While it protected mice from colon cancer in a model of inflammation-triggered carcinogenesis (azoxymethane and dextran sodium sulfate treatment), it promoted growth of xenografted tumor cells. Therefore, we analyzed the effect of GPx2 in a mouse model mimicking sporadic colorectal cancer (azoxymethane-treatment only). GPx2-knockout (KO) and wild-type (WT) mice were adjusted to an either marginally deficient (-Se), adequate (+Se), or supranutritional (++Se) selenium status and were treated six times with azoxymethane (AOM) to induce tumor development. In the -Se and ++Se groups, the number of tumors was significantly lower in GPx2-KO than in respective WT mice. On the +Se diet, the number of dysplastic crypts was reduced in GPx2-KO mice. This may be explained by more basal and AOM-induced apoptotic cell death in GPx2-KO mice that eliminates damaged or pre-malignant epithelial cells. In WT dysplastic crypts GPx2 was up-regulated in comparison to normal crypts which might be an attempt to suppress apoptosis. In contrast, in the +Se groups tumor numbers were similar in both genotypes but tumor size was larger in GPx2-KO mice. The latter was associated with an inflammatory and tumor-promoting environment as obvious from infiltrated inflammatory cells in the intestinal mucosa of GPx2-KO mice even without any treatment and characterized as low-grade inflammation. In WT mice the number of tumors tended to be lowest in +Se compared to -Se and ++Se feeding indicating that selenium might delay tumorigenesis only in the adequate status. In conclusion, the role of GPx2 and presumably also of selenium depends on the cancer stage and obviously on the involvement of inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.