ArticleBioMed research international2015
Ras oncogene-mediated progressive silencing of extracellular superoxide dismutase in tumorigenesis.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- ERK2 Is a Promoter of Cancer Cell Growth and Migration in Colon Adenocarcinoma.Antioxidants (Basel, Switzerland) · 2024Article
- Thyroid Cancer and Fibroblasts.Cancers · 2022Review
- The Effect of Extracellular Superoxide Dismutase (SOD3) Gene in Lung Cancer.Frontiers in oncology · 2022Article
- SOD3 Is a Non-Mutagenic Growth Regulator Affecting Cell Migration and Proliferation Signal Transduction.Antioxidants (Basel, Switzerland) · 2021Article
- HAntioxidants (Basel, Switzerland) · 2019Review
- Carcinogenesis and Reactive Oxygen Species Signaling: Interaction of the NADPH Oxidase NOX1-5 and Superoxide Dismutase 1-3 Signal Transduction Pathways.Antioxidants & redox signaling · 2019Review
- Extracellular superoxide dismutase and its role in cancer.Free radical biology & medicine · 2017Review
- Statin and Bisphosphonate Induce Starvation in Fast-Growing Cancer Cell Lines.International journal of molecular sciences · 2017Article
- Extracellular Superoxide Dismutase Expression in Papillary Thyroid Cancer Mesenchymal Stem/Stromal Cells Modulates Cancer Cell Growth and Migration.Scientific reports · 2017Article
- PATZ1 is a target of miR-29b that is induced by Ha-Ras oncogene in rat thyroid cells.Scientific reports · 2016Article
- Extracellular Superoxide Dismutase: Growth Promoter or Tumor Suppressor?Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular superoxide dismutase (SOD3) is a secreted enzyme that uses superoxide anion as a substrate in a dismutase reaction that results in the formation of hydrogen peroxide. Both of these reactive oxygen species affect growth signaling in cells. Although SOD3 has growth-supporting characteristics, the expression of SOD3 is downregulated in epithelial cancer cells. In the current work, we studied the mechanisms regulating SOD3 expression in vitro using thyroid cell models representing different stages of thyroid cancer. We demonstrate that a low level of RAS activation increases SOD3 mRNA synthesis that then gradually decreases with increasing levels of RAS activation and the decreasing degree of differentiation of the cancer cells. Our data indicate that SOD3 regulation can be divided into two classes. The first class involves RAS-driven reversible regulation of SOD3 expression that can be mediated by the following mechanisms: RAS GTPase regulatory genes that are responsible for SOD3 self-regulation; RAS-stimulated p38 MAPK activation; and RAS-activated increased expression of the mir21 microRNA, which inversely correlates with sod3 mRNA expression. The second class involves permanent silencing of SOD3 mediated by epigenetic DNA methylation in cells that represent more advanced cancers. Therefore, the work suggests that SOD3 belongs to the group of ras oncogene-silenced genes.
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