ArticleOncology letters2015
Effect of camptothecin on inducible nitric oxide synthase expression in the colon cancer SW480 cell line.
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Gasotransmitters in the tumor microenvironment: Impacts on cancer chemotherapy (Review).Molecular medicine reports · 2022Review
- Camptothecin Encapsulated in β-Cyclodextrin-EDTA-FeNanomaterials (Basel, Switzerland) · 2021Article
- Inverse Association between Glucose‒6‒Phosphate Dehydrogenase Deficiency and Hepatocellular CarcinomaAsian Pacific journal of cancer prevention : APJCP · 2018Article
- Efficiency of newly formulated camptothecin with β-cyclodextrin-EDTA-FeScientific reports · 2017Article
- Glucose-6-phosphate dehydrogenase deficiency and risk of colorectal cancer in Northern Sardinia: A retrospective observational study.Medicine · 2016Observational
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a topoisomerase I inhibitor, camptothecin (CPT) is regarded as an effective antitumor agent. In an attempt to search for its novel anticancer mechanism, the present study evaluated the effects of CPT on inducible nitric oxide synthase (iNOS) in the human colon cancer SW480 cell line when stimulated with lipopolysaccharide (LPS) and interleukin (IL)-1β. The data indicated that CPT significantly decreased NO production. Consistent with these observations, the protein and mRNA expression levels of iNOS were inhibited by CPT in a dose-dependent manner. Thus, the inhibitory effects of CPT on LPS/IL-1β-stimulated NO production were likely mediated via the inhibition of iNOS gene transcription. From these results, we propose that the inhibition of NO biosynthesis by CPT may partially underlie the efficacy of this antitumor agent.
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