ArticleThe Kaohsiung journal of medical sciences2020
The anti-infection drug furazolidone inhibits NF-κB signaling and induces cell apoptosis in small cell lung cancer.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Small Schiff Base Molecules-A Possible Strategy to Combat Biofilm-Related Infections.Antibiotics (Basel, Switzerland) · 2024Review
- Anti-proliferative effects of the combination of Sulfamethoxazole and Quercetin via caspase3 and NFkB gene regulation: an in vitro and in vivo study.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Identification of Potential Biomarkers and Small Molecule Drugs for Cutaneous Melanoma Using Integrated Bioinformatic Analysis.Frontiers in cell and developmental biology · 2022Article
- Molecular Characteristics of m6A Regulators and Tumor Microenvironment Infiltration in Soft Tissue Sarcoma: A Gene-Based Study.Frontiers in bioengineering and biotechnology · 2022Article
- Transcriptional Modulation of the Hippo Signaling Pathway by Drugs Used to Treat Bipolar Disorder and Schizophrenia.International journal of molecular sciences · 2021Article
- The anti-infection drug furazolidone inhibits NF-κB signaling and induces cell apoptosis in small cell lung cancer.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Targeting nuclear factor kappa B (NF-κB) signaling pathway has become a promising strategy for the development of new antitumor drugs. In this paper, we found that anti-infection drug furazolidone (FZD) could significantly inhibit NF-κB-driven luciferase activity, and FZD could markedly inhibit both of the constitutive and tumor necrosis factor-α (TNFα)-triggered phosphorylation of NF-κB p65 in small cell lung cancer (SCLC). Further studies revealed that FZD inhibited the expression of inhibitor of kappa B kinase β (IKKβ) in SCLC cells. In addition, we found that FZD had significant antitumor activities in SCLC cells. FZD could markedly suppress the cell viability of SCLC cells dose-dependently, and FZD could significantly induce the cleavages of poly ADP-ribose polymerase (PARP) and Caspase3, the biomarkers of cell apoptosis, in SCLC cells. The flow cytometry also revealed that FZD induced cell apoptosis in SCLC cells. Finally, we also found that overexpression of constitutively activated IKKβ could significantly abolish FZD-induced cell growth inhibition in SCLC cells, which further confirmed that FZD displayed its anti-SCLC activity through regulating NF-κB signaling pathway.
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