ArticleCell proliferation2020
IL-6 promotes metastasis of non-small-cell lung cancer by up-regulating TIM-4 via NF-κB.
Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 137 citations in OpenAlex.
- IL-6/IL-6R-Mediated Mechanisms in Lung Cancer: From Pathogenesis to Potential Therapeutic Targets.Immunology · 2026Review
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Exosomal 3'tiRNA-PheGAA and interleukin-6 as novel biomarkers for non-invasive detection of NSCLC.Discover oncology · 2026Article
- The role of macrophages and cytokines in the occurrence and development of MDS.Clinical and experimental medicine · 2026Review
- In-depth Evaluation of the Olink Target 48 Cytokine Panel: Inter-Laboratory Evaluation of Performance and Reliability for Biomarker Studies in Oncology.The AAPS journal · 2026Article
- Infiltration of TIM4-positive intratumoral macrophages serves as an adverse prognostic factor in breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- Cellular senescence in lung cancer immune microenvironment and senotherapeutic opportunities.iScience · 2026Review
- Macrophage and IL-6 signaling modulate multiple myeloma progression and response to metformin and CAR-T cell therapy.Frontiers in immunology · 2026Article
- Pathogenic role and therapeutic targets of nuclear factor-κB signaling pathway in cancer (Review).Oncology letters · 2025Review
- Role of signaling pathways in lung cancer development and advances in targeted therapies (Review).Oncology letters · 2025Review
- RBMX2 linkseLife · 2025Article
- Dietary ω-3 polyunsaturated fatty acids (PUFAs) reduce cholesterol-driven non-small cell lung cancer (NSCLC) progression in mouse models of disease.Communications medicine · 2025Article
- WNK1 promotes head and neck squamous cell carcinoma progression through activation of NF-κB signaling pathway.Discover oncology · 2025Article
- Overlapping risk factors and pathogenic mechanisms in lung cancer and cardiovascular disease.Discover oncology · 2025Review
- Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review.Cancer cell international · 2025Review
- Article
- Lung cancer intravasation-on-a-chip: Visualization and machine learning-assisted automatic quantification.Bioactive materials · 2025Article
- Oxidative Stress and Inflammation: Drivers of Tumorigenesis and Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2025Review
- The Diverse Function of IL-6 in Biological Processes and the Advancement of Cancer.Immune network · 2025Review
- Exploring the cancerous nexus: the pivotal and diverse roles of USP39 in cancer development.Discover oncology · 2025Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesInterleukin-6 (IL-6) is critical for the development of non-small-cell lung cancer (NSCLC). Recently, we identified T-cell immunoglobulin domain and mucin domain 4 (TIM-4) as a new pro-growth player in NSCLC progression. However, the role of TIM-4 in IL-6-promoted NSCLC migration, invasion and epithelial-to-mesenchymal transition (EMT) remains unclear. MATERIALS AND
methodsExpressions of TIM-4 and IL-6 were both evaluated by immunohistochemical staining in NSCLC tissues. Real-time quantitative PCR (qPCR), Western blot, flow cytometry and RT-PCR were performed to detect TIM-4 expression in NSCLC cells with IL-6 stimulation. The roles of TIM-4 in IL-6 promoting migration and invasion of NSCLC were detected by transwell assay. EMT-related markers were analysed by qPCR and Western blot in vitro, and metastasis was evaluated in BALB/c nude mice using lung cancer metastasis mouse model in vivo.
resultsHigh IL-6 expression was identified as an independent predictive factor for TIM-4 expression in NSCLC tissues. NSCLC patients with TIM-4 and IL-6 double high expression showed the worst prognosis. IL-6 promoted TIM-4 expression in NSCLC cells depending on NF-κB signal pathway. Both TIM-4 and IL-6 promoted migration, invasion and EMT of NSCLC cells. Interestingly, TIM-4 knockdown reversed the role of IL-6 in NSCLC and IL-6 promoted metastasis of NSCLC by up-regulating TIM-4 via NF-κB.
conclusionsTIM-4 involves in IL-6 promoted migration, invasion and EMT of NSCLC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.