ArticleInternational journal of biological sciences2019
An Autocrine IL-6/IGF-1R Loop Mediates EMT and Promotes Tumor Growth in Non-small Cell Lung Cancer.
Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- IL-6/IL-6R-Mediated Mechanisms in Lung Cancer: From Pathogenesis to Potential Therapeutic Targets.Immunology · 2026Review
- Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026Review
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- STAT3 signaling mediates EGFR-TKI resistance in non-small cell lung cancer by regulating stemness markers and telomerase, reversed by icaritin.British journal of cancer · 2026Article
- IL‑6: A key player in the EGFR‑TKI‑resistant tumor microenvironment and its therapeutic implications (Review).International journal of oncology · 2026Review
- Association between four indirect indicators of insulin resistance and lung cancer: evidence from UK biobank and Mendelian randomization analysis.BMC cancer · 2026Article
- IGF-1R inhibitors in cancer: A review of available evidence and future outlook.Critical reviews in oncology/hematology · 2025Review
- Role of interleukin-6 in resistance to tumor therapy.Discover oncology · 2025Review
- IL-6 promotes metastasis and EMT of non-small cell lung cancer cells by up-regulating FGL1 via STAT3 pathway.Translational cancer research · 2025Article
- Molecular mechanisms of the Xiao-chai-hu-tang on chronic stress-induced colorectal cancer growth based on an integrated network pharmacology and RNA sequencing approach with experimental validation.BMC complementary medicine and therapies · 2025Article
- Shenqi Fuzheng injection restores the sensitivity to gefitinib in non-small cell lung cancer by inhibiting the IL-22/STAT3/AKT pathway.Pharmaceutical biology · 2024Article
- [Progress in the Study of Mechanisms Clinically Relevant to Insulin Resistance and Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Tumor-associated macrophages/C-X-C motif chemokine ligand 1 promotes breast cancer autophagy-mediated chemoresistance via IGF1R/STAT3/HMGB1 signaling.Cell death & disease · 2024Article
- Role of PATJ in stroke prognosis by modulating endothelial to mesenchymal transition through the Hippo/Notch/PI3K axis.Cell death discovery · 2024Article
- Gold Nanoparticles Downregulate IL-6 Expression/Production by Upregulating microRNA-26a-5p and Deactivating the RelA and NF-κBp50 Transcription Pathways in Activated Breast Cancer Cells.International journal of molecular sciences · 2024Article
- A review on potential heterocycles for the treatment of glioblastoma targeting receptor tyrosine kinases.Oncology research · 2024Review
- A combined preoperative red cell distribution width and carcinoembryonic antigen score contribute to prognosis prediction in stage I lung adenocarcinoma.World journal of surgical oncology · 2023Article
- Mutual connected IL-6, EGFR and LIN28/Let7-related mechanisms modulate PD-L1 and IGF upregulation in HNSCC using immunotherapy.Frontiers in oncology · 2023Review
- Bioactive PI3-kinase/Akt/mTOR Inhibitors in Targeted Lung Cancer Therapy.Advanced pharmaceutical bulletin · 2023Review
- IGF-1 Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells That Is Conferred by miR-3666 Loss.Contrast media & molecular imaging · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) is a key process in EGFR-TKI resistance but the detailed mechanism is largely unknown. We aim to evaluate the role of interleukin-6 (IL-6) and insulin-like growth factor-1 receptor (IGR-1R) in EMT in non-small cell lung cancer (NSCLC). We used IL-6 to induce EMT in EGFR-TKI sensitive NSCLC cells. We found that both STAT3 and IGF-1R were activated. Interestingly activation of STAT3 and JAK1 was blocked by inhibiting IGF-1R, suggesting that IGF-1R might signal via JAK/STAT3. Activation of IGF-1R and AKT was inhibited by blocking STAT3, suggesting that STAT3 blockade might provide negative feedback signal to inhibiting IGF-1R. Reporter assay further confirmed that STAT3 activated gene transcription of IGF-1R. RT-PCR analyses showed that IL-6 induced the expression of IL-6 per se as well as IGF-1 and IGF-2. Expression of IL-6 and IGF-1R ligands was suppressed by inhibiting either STAT3 or IGF-1R. Meanwhile IL-6 induced gefitinib resistance and increased migration. We elucidated an autocrine loop of IL-6/IGF-1R/STAT3 in EMT-mediated resistance and tumor growth in NSCLC.
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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.