ArticleCancer cell international2018
Interferon-γ and Smac mimetics synergize to induce apoptosis of lung cancer cells in a TNFα-independent manner.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Effects of moxibustion therapies on immune function in cancer animal models: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- Tumor microenvironment-driven immune evasion in triple-negative breast cancer: mechanisms, clinical challenges, and therapeutic opportunities.Frontiers in immunology · 2026Review
- The difference in tumor immune microenvironment and IFN-γ response between solid and non-solid adenocarcinoma.Translational lung cancer research · 2025Article
- Uncovering the rewired IAP-JAK regulatory axis as an immune-dependent vulnerability of LKB1-mutant lung cancer.Nature communications · 2025Article
- Exploring causal relationship between 41 inflammatory cytokines and marginal zone lymphoma: A bidirectional Mendelian randomization study.Open medicine (Warsaw, Poland) · 2025Article
- Synergistic effects of Smac mimetic APG-1387 with anti-PD-1 antibody are attributed to increased CD3 + NK1.1 + cell recruitment secondary to induction of cytokines from tumor cells.Cancer cell international · 2024Article
- Implications of NLRP3 Suppression Using Glibenclamide and miR-223 against Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Iron and copper: critical executioners of ferroptosis, cuproptosis and other forms of cell death.Cell communication and signaling : CCS · 2023Review
- Current literature review on the tumor immune micro-environment, its heterogeneity and future perspectives in treatment of advanced non-small cell lung cancer.Translational lung cancer research · 2023Review
- Crosstalk of Inflammatory Cytokines within the Breast Tumor Microenvironment.International journal of molecular sciences · 2023Review
- UBR5 promotes tumor immune evasion through enhancing IFN-γ-inducedTheranostics · 2022Article
- BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021Review
- The Smac mimetic BV6 cooperates with STING to induce necroptosis in apoptosis-resistant pancreatic carcinoma cells.Cell death & disease · 2021Article
- miR-20b and miR-125a promote tumorigenesis in radioresistant esophageal carcinoma cells.Aging · 2021Article
- The role ofTranslational cancer research · 2021Article
- The CXCL Family Contributes to Immunosuppressive Microenvironment in Gliomas and Assists in Gliomas Chemotherapy.Frontiers in immunology · 2021Article
- RIPK1 polymorphisms alter the susceptibility to cervical Cancer among the Uyghur population in China.BMC cancer · 2020Article
- The Immuno-Modulatory Effects of Inhibitor of Apoptosis Protein Antagonists in Cancer Immunotherapy.Cells · 2020Review
- Roles of IFN-γ in tumor progression and regression: a review.Biomarker research · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe prognosis of lung cancer is very poor and hence new therapeutic strategies are urgently desired. In this study, we searched for efficacious Smac mimetic-based combination therapies with biomarkers to predict responses for non-small cell lung cancer (NSCLC).
methodsNSCLC cell lines and normal human alveolar epithelial cells were treated with Smac mimetics plus IFNγ or other agonists and cell viabilities were assessed by MTS assay, cell counting, flow cytometry and cell colony assay. Western blot analysis was performed to assess the cleavage (activation) of caspases and expression of signaling molecules. Caspase activity was determined to verify caspase activation. The pathways involved in NSCLC cell death were investigated using specific inhibitors.
resultsWe found that IFNγ could cooperate with various Smac mimetics to trigger a profound apoptosis in a number of NSCLC cell lines that are competent for IFNγ signaling (i.e. expressing IFNγ receptor-1 and STAT1) but have low expression levels of inhibitor of apoptosis proteins survivin and livin without harming normal human lung epithelial cells. IFNγ co-treatment with a novel class dimeric Smac mimetic AZD5582 eradicated NSCLC cell colony formation. Unlike IFNγ, IFNα, IFNλ, TNFα, or TRAIL alone or plus AZD5582 had minor effects on NSCLC cell viability. IFNγ/AZD5582-induced cell death in NSCLC cells was independent of TNFα autocrine but relied on apoptosis mediated by JAK kinase, caspase 8 and RIPK1 pathways.
conclusionOur results indicate that IFNγ and Smac mimetics can synergize to induce apoptosis of NSCLC cells and suggest that IFNγ and Smac mimetic regimen may be a novel and efficacious apoptosis targeted therapy with biomarkers to predict responses for NSCLC cells.
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