ArticleCancer science2013
Arsenic trioxide prevents nitric oxide production in lipopolysaccharide -stimulated RAW 264.7 by inhibiting a TRIF-dependent pathway.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Arsenic attenuates responsiveness to inflammatory stimuli in the SIM-A9 microglial cell line.Neurotoxicology · 2026Article
- Human RP105 monoclonal antibody enhances antigen-specific antibody production in unique culture conditions.iScience · 2024Article
- Novel Interleukin-6 Inducible Gene PDZ-Binding Kinase Promotes Tumor Growth of Multiple Myeloma Cells.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2020Article
- Biallelic loss of FAM46C triggers tumor growth with concomitant activation of Akt signaling in multiple myeloma cells.Cancer science · 2020Article
- Establishment and characterization of a novel vincristine-resistant diffuse large B-cell lymphoma cell line containing the 8q24 homogeneously staining region.FEBS open bio · 2018Article
- Double-Sided Personality: Effects of Arsenic Trioxide on Inflammation.Inflammation · 2018Review
- Novel ATP-competitive Akt inhibitor afuresertib suppresses the proliferation of malignant pleural mesothelioma cells.Cancer medicine · 2017Article
- Molecular insight of arsenic-induced carcinogenesis and its prevention.Naunyn-Schmiedeberg's archives of pharmacology · 2017Review
- Δ40p53α suppresses tumor cell proliferation and induces cellular senescence in hepatocellular carcinoma cells.Journal of cell science · 2017Article
- The Potential Role of Nitric Oxide in Halting Cancer Progression Through Chemoprevention.Journal of cancer prevention · 2016Review
- Lipopolysaccharide augments the uptake of oxidized LDL by up-regulating lectin-like oxidized LDL receptor-1 in macrophages.Molecular and cellular biochemistry · 2015Article
- Recognition of LPS by TLR4: potential for anti-inflammatory therapies.Marine drugs · 2014Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arsenic trioxide (ATO) is one of the most potent drugs in cancer chemotherapy, and is highly effective in treating both newly diagnosed and relapse patients with acute promyelocytic leukemia (APL). Despite a number of reports regarding the molecular mechanisms by which ATO promotes anti-tumor or pro-apoptotic activity in hematological and other solid malignancies, the effects of ATO on immune responses remain poorly understood. To further understand and clarify the effects of ATO on immune responses, we sought to examine whether ATO affects the production of nitric oxide (NO) in a lipopolysaccharide (LPS)-stimulated mouse macrophage cell line, RAW 264.7. Arsenic trioxide was found to prevent NO production in a dose-dependent manner. Arsenic trioxide significantly inhibited the increase in inducible nitric oxide synthase (iNOS) at both the mRNA and protein levels. Furthermore, our analyses revealed that the inhibitory effect of ATO on iNOS expression was ascribed to the prevention of IRF3 phosphorylation, interferon (IFN)-β expression, and STAT1 phosphorylation, but not the prevention of the MyD88-dependent pathway. Taken together, our results indicate that ATO prevents NO production by inhibiting the TIR-domain-containing adaptor protein inducing IFN-β (TRIF)-dependent pathway, thus highlighting an anti-inflammatory property of ATO in innate immunity.
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