ArticleMolecular carcinogenesis2013
Regulation of pancreatic cancer growth by superoxide.
Article in Molecular carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Inflammation and RONS Dysregulation by Redox Enzymes as Mechanistic Links in HIV-1-Cancer Comorbidity.Pathogens (Basel, Switzerland) · 2026Review
- Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Nicotinamide adenine dinucleotide phosphate oxidase in pancreatic diseases: Mechanisms and future perspectives.World journal of gastroenterology · 2024Review
- Hydrogen Peroxide Mediates Pharmacological Ascorbate Induced Radio-Sensitization of Pancreatic Cancer Cells by Enhancing G2-accumulation and Reducing Cyclin B1 Protein Levels.Radiation research · 2023Article
- Crosstalk Between ROS and Autophagy in Tumorigenesis: Understanding the Multifaceted Paradox.Frontiers in oncology · 2022Review
- Impact of EcSOD Perturbations in Cancer Progression.Antioxidants (Basel, Switzerland) · 2021Review
- Catalase Modulates the Radio-Sensitization of Pancreatic Cancer Cells by Pharmacological Ascorbate.Antioxidants (Basel, Switzerland) · 2021Article
- Pharmacological ascorbate inhibits pancreatic cancer metastases via a peroxide-mediated mechanism.Scientific reports · 2020Article
- Cannabidiol and Oxygen-Ozone Combination Induce Cytotoxicity in Human Pancreatic Ductal Adenocarcinoma Cell Lines.Cancers · 2020Article
- The latency of peroxisomal catalase in terms of effectiveness factor for pancreatic and glioblastoma cancer cell lines in the presence of high concentrations of HFree radical biology & medicine · 2020Article
- Increased formation of reactive oxygen species during tumor growth: Ex vivo low-temperature EPR and in vivo bioluminescence analyses.Free radical biology & medicine · 2020Article
- Duox1 Regulates Primary B Cell Function under the Influence of IL-4 through BCR-Mediated Generation of Hydrogen Peroxide.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Metabolism-Based Therapeutic Strategies Targeting Cancer Stem Cells.Frontiers in pharmacology · 2019Review
- Enhanced Pharmacological Ascorbate Oxidation Radiosensitizes Pancreatic Cancer.Radiation research · 2019Article
- Treating pancreatic cancer: more antioxidants more problems?Expert review of gastroenterology & hepatology · 2018Review
- The plasticity of pancreatic cancer metabolism in tumor progression and therapeutic resistance.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- Superoxide Dismutases in Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2017Review
- Article
- Targeting reactive oxygen species in development and progression of pancreatic cancer.Expert review of anticancer therapy · 2017Review
- Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
K-ras mutations have been identified in up to 95% of pancreatic cancers, implying their critical role in the molecular pathogenesis. Expression of K-ras oncogene in an immortalized human pancreatic ductal epithelial cell line, originally derived from normal pancreas (H6c7), induced the formation of carcinoma in mice. We hypothesized that K-ras oncogene correlates with increased non-mitochondrial-generated superoxide (O 2.-), which could be involved in regulating cell growth contributing to tumor progression. In the H6c7 cell line and its derivatives, H6c7er-Kras+ (H6c7 cells expressing K-ras oncogene), and H6c7eR-KrasT (tumorigenic H6c7 cells expressing K-ras oncogene), there was an increase in hydroethidine fluorescence in cell lines that express K-ras. Western blots and activity assays for the antioxidant enzymes that detoxify O 2.- were similar in these cell lines suggesting that the increase in hydroethidine fluorescence was not due to decreased antioxidant capacity. To determine a possible non-mitochondrial source of the increased levels of O 2.-, Western analysis demonstrated the absence of NADPH oxidase-2 (NOX2) in H6c7 cells but present in the H6c7 cell lines expressing K-ras and other pancreatic cancer cell lines. Inhibition of NOX2 decreased hydroethidine fluorescence and clonogenic survival. Furthermore, in the cell lines with the K-ras oncogene, overexpression of superoxide dismutases that detoxify non-mitochondrial sources of O 2.-, and treatment with the small molecule O 2.- scavenger Tempol, also decreased hydroethidine fluorescence, inhibited clonogenic survival and inhibited growth of tumor xenografts. Thus, O 2.- produced by NOX2 in pancreatic cancer cells with K-ras, may regulate pancreatic cancer cell growth.
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Registered trials
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