ArticleAmerican journal of cancer research2015
Interleukin-17-induced EMT promotes lung cancer cell migration and invasion via NF-κB/ZEB1 signal pathway.
Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 105 citations in OpenAlex.
- Regulatory role of IL-17-mediated inflammatory pathways in lung cancer initiation and progression.Discover oncology · 2026Review
- Emodin inhibits breast tumorigenesis in the comorbidity of hyperlipidemia and associated with IL-17 suppression.Biochemistry and biophysics reports · 2026Article
- "Cytokine-Mediated tumor sensitization: mechanistic frameworks and therapeutic opportunities in cancer Immunotherapy".Clinical and experimental medicine · 2026Review
- cPLACytotechnology · 2025Article
- Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- ZEB1 expression in Th17 cells correlated with p-STAT3 in human apical periodontitis.BMC oral health · 2025Article
- Unlocking melanoma Suppression: Insights from Plasma-Induced potent miRNAs through PI3K-AKT-ZEB1 axis.Journal of advanced research · 2025Article
- Role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer (Review).Oncology reports · 2024Review
- Optimization of In Vitro Th17 Polarization for Adoptive Cell Therapy in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2024Article
- Decreased interleukin-17RA expression is associated with good prognosis in patients with colorectal cancer and inhibits tumor growth and vascularity in mice.Cancer medicine · 2024Article
- The role of interleukin-17 in inflammation-related cancers.Frontiers in immunology · 2024Review
- The Nexus of Inflammation-Induced Epithelial-Mesenchymal Transition and Lung Cancer Progression: A Roadmap to Pentacyclic Triterpenoid-Based Therapies.International journal of molecular sciences · 2023Review
- IL-17A promotes tumorigenesis and upregulates PD-L1 expression in non-small cell lung cancer.Journal of translational medicine · 2023Article
- Notopterol Suppresses IL-17-Induced Proliferation and Invasion of A549 Lung Adenocarcinoma Cells via Modulation of STAT3, NF-κB, and AP-1 Activation.International journal of molecular sciences · 2023Article
- Involvement of Epithelial-Mesenchymal Transition (EMT) in Autoimmune Diseases.International journal of molecular sciences · 2023Review
- Respiratory Syncytial Virus Infection Does Not Induce Epithelial-Mesenchymal Transition.Journal of virology · 2023Article
- The role of Th17 cells in chronic lymphocytic leukemia: friend or foe?Blood advances · 2023Review
- Unpacking the Complexity of Epithelial Plasticity: From Master Regulator Transcription Factors to Non-Coding RNAs.Cancers · 2023Review
- Review
- Neural crest E-cadherin loss drives cleft lip/palate by epigenetic modulation via pro-inflammatory gene-environment interaction.Nature communications · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory cytokine interleukin-17 (IL-17) has been associated with the risk of progressive cancers including lung cancer. However, it remains unclear how IL-17 may contribute to the invasion and development of these inflammation-associated malignancies. Here we aimed to investigate the role of IL-17 in lung cancer cell development. Epithelial-mesenchymal transition (EMT) has been recently proposed as a developmental process which plays an important role in cancer progression and metastases. Here we show that IL-17 might promote EMT in lung cancer cells by inducing the transcriptional repressor ZEB1. Exposure to IL-17 upregulated the signature EMT phenotypic markers vimentin and E-cadherin in lung cancer cells, and compared with controls, increased cell migration was observed in IL-17-treated lung cancer cells. ZEB1 mRNA and protein expression was induced by IL-17, and IL-17 stimulated nuclear localization of phosphorylated ZEB1. Conversely, suppressing ZEB1 expression by ZEB1 siRNA abrogated IL-17-stimulated vimentin expression and cell migration. Moreover, the phosphorylation of IκBα was required for IL-17-induced expression of ZEB1, suggesting the involvement of canonical NF-κB signaling. To check this hypothesis, we used IKK inhibitor BAY 11-7028 to block NF-κB activity. We found that BAY 11-7028 abrogated IL-17-induced ZEB1 expression, cell migration, and EMT, thus confirming that NF-κB is required for IL-17 to induce these aggressive phenotypes in lung cancer cells. Taken together, our data support the idea that IL-17-induced EMT promotes lung cancer cell migration and invasion via NF-κB-mediated upregulation of ZEB1. This study reveals a new signaling axis through which the tumor microenvironment causes ZEB1 expression to promote cancer metastasis. We suggest that targeting IL-17-induced ZEB1 expression may offer an effective therapeutic strategy for lung cancer treatment.
Indexed as
Identifiers
26045995PMC4449444W2275445498What OpenQuestion holds
Registered trials
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.