ArticleScientific reports2021
Golden berry 4β-hydroxywithanolide E prevents tumor necrosis factor α-induced procoagulant activity with enhanced cytotoxicity against human lung cancer cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 23 citations in OpenAlex.
- Panduratin A Induces Caspase-Dependent Apoptosis and G1-Associated Cell-Cycle Arrest and Enhances TNF-α-Associated Cytotoxicity in NSCLC Cells.Biomolecules · 2026Article
- The seven human coronavirus main proteases exhibit differential modulation of NF-κB suppression via TAB1 cleavage.Communications biology · 2026Article
- Identification of costimulatory molecule signatures for evaluating prognostic risk in non-small cell lung cancer.Heliyon · 2024Article
- Management of triple-negative breast cancer by natural compounds through different mechanistic pathways.Frontiers in genetics · 2024Review
- Impact of daily administration of blackberry extract on gerbil model of transient cerebral ischemia.Acta cirurgica brasileira · 2024Article
- Hairy root culture: a potent method for improved secondary metabolite production of Solanaceous plants.Frontiers in plant science · 2023Review
- Recent Studies on Berry Bioactives and Their Health-Promoting Roles.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation in the tumor microenvironment is positively correlated with cancer progression and metastasis as well as the risk of thromboembolism in lung cancer patients. Here we show, in human non-small cell lung cancer (NSCLC) cell lines, the master inflammatory cytokine tumor necrosis factor (TNF-α) induced tissue factor expression and procoagulant activity, and these effects were potently inhibited by 4β-hydroxywithanolide E (4HW), a natural compound isolated from Physalis peruviana. Furthermore, combination of 4HW and TNF-α caused synergistic cytotoxicity against NSCLC cells by inducing caspase-dependent apoptosis. The underlying mechanism by which 4HW reverses the procoagulant effect of TNF-α but enhances its cytotoxic effect appears to be due to inhibition of NF-κB, which is a key switch for both inflammation-induced coagulation and cell survival. Our results suggest that 4HW may have a potential application for treating inflammation-derived cancer progression and cancer-associated hypercoagulable state.
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