ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
The CCL2/CCR2 axis enhances IL-6-induced epithelial-mesenchymal transition by cooperatively activating STAT3-Twist signaling.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 72 citations in OpenAlex.
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- The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials.Frontiers in immunology · 2026Review
- P2X4 purinergic receptor loss alters macrophage homeostasis, cytokine secretion, and phagocytosis in a myeloid-specific P2X4 purinergic receptor knockout mouse.Frontiers in immunology · 2026Article
- Activation of the NALP3-CASP1-IL-1 β Inflammatory Pathway by Pesticide Exposure in Human Umbilical Vein Endothelial Cells.International journal of molecular sciences · 2025Article
- The IL-6/JAK/STAT3 Axis in Cholangiocarcinoma and Primary Sclerosing Cholangitis: Unlocking Therapeutic Strategies Through Patient-Derived Organoids.Biomedicines · 2025Article
- The role and clinical significance of tumor-associated macrophages in the epithelial-mesenchymal transition of lung cancer.Frontiers in oncology · 2025Review
- Glucocorticoid boluses followed by tocilizumab in giant cell arteritis patients: effects on peripheral blood monocytes and lymphocytes.Frontiers in immunology · 2025Article
- Relationship between adipocytes and hematological tumors in the bone marrow microenvironment: a literature review.Translational cancer research · 2024Review
- Interleukin 6 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 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
- A hybrid breast cancer/mesenchymal stem cell population enhances chemoresistance and metastasis.JCI insight · 2023Article
- Ethnic disparities in the immune microenvironment of triple negative breast cancer and its role in therapeutic outcomes.Cancer reports (Hoboken, N.J.) · 2023Review
- Dissecting the effects of androgen deprivation therapy on cadherin switching in advanced prostate cancer: A molecular perspective.Oncology research · 2022Review
- Role of the CCL2-CCR2 signalling axis in cancer: Mechanisms and therapeutic targeting.Cell proliferation · 2021Review
- Claudin-Low Breast Cancer Inflammatory Signatures Support Polarization of M1-Like Macrophages with Protumoral Activity.Cancers · 2021Article
- Co-Targeting PIM Kinase and PI3K/mTOR in NSCLC.Cancers · 2021Article
- Exploring the Crosstalk between Inflammation and Epithelial-Mesenchymal Transition in Cancer.Mediators of inflammation · 2021Review
- Is the C-C Motif Ligand 2-C-C Chemokine Receptor 2 Axis a Promising Target for Cancer Therapy and Diagnosis?International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pattern of secreted factors in the tumor microenvironment has been shown to initiate tumor epithelial-mesenchymal transition (EMT); however, little is known about their interplay undergoing this phenotypic switch. In this study, we revealed obvious coactions of cytokine IL-6 and chemokine CCL2 during EMT induction. We found that IL-6 effectively induced EMT and promoted tumor cell invasion, which could be markedly enhanced by addition of CCL2 in a CCR2-dependent manner. IL-6 and CCL2 induced each other and cooperatively elicited STAT3 phosphorylation; conversely, STAT3 regulated the production of IL-6 and CCL2, thus constituting a positive feedback loop to maintain and amplify STAT3 signaling, consequently promoting additional EMT events. Furthermore, CCL2 greatly enhanced IL-6-induced EMT events mainly by upregulating the expression of Twist. Genetic or pharmacological inhibition of STAT3 disrupted STAT3-centered loop and markedly suppressed Twist expression as well as IL-6/CCL2-mediated EMT induction. Thus, our findings highlighted the synergy of the two secreted factors of tumor microenvironment, in regulating transformed properties of non-small cell lung cancer (NSCLC).
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