ArticleJournal of cellular and molecular medicine2019
Reciprocal regulation of miR-206 and IL-6/STAT3 pathway mediates IL6-induced gefitinib resistance in EGFR-mutant lung cancer cells.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- IL-6/IL-6R-Mediated Mechanisms in Lung Cancer: From Pathogenesis to Potential Therapeutic Targets.Immunology · 2026Review
- Activation of the NF-κB/ALDH1A1 signaling promotes non-mutational resistance to EGFR-TKIs in non-small cell lung cancer.Oncogene · 2026Article
- Humanized Antibodies Targeting Ectodomains of IL-6R and GP130 Suppress IL-6/STAT3 Signalling and Tumour Growth in Breast Cancer Models.Journal of cellular and molecular medicine · 2026Article
- IL‑6: A key player in the EGFR‑TKI‑resistant tumor microenvironment and its therapeutic implications (Review).International journal of oncology · 2026Review
- Role of interleukin-6 in resistance to tumor therapy.Discover oncology · 2025Review
- CRISPR-mediated WNK4 point mutation aggravates tumor progression and weakens chemotherapy sensitivity in gastric cancer.Histology and histopathology · 2025Article
- The Role and Therapeutic Potential of Non-coding RNAs in Resistance to EGFR - TKIs Targeted Therapy for Non-small Cell Lung Cancer.Current medicinal chemistry · 2025Review
- MicroRNA-130a-3p regulates osimertinib resistance by targeting runt-related transcription factor 3 in lung adenocarcinoma.Scientific reports · 2024Article
- Multi-omics analysis of macrophage-associated receptor and ligand reveals a strong prognostic signature and subtypes in hepatocellular carcinoma.Scientific reports · 2024Article
- Identification of biomarkers, pathways, and therapeutic targets for EGFR-TKI resistance in NSCLC.Life science alliance · 2023Article
- Circulating miR-206 and miR-1246 as Markers in the Early Diagnosis of Lung Cancer in Patients with Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2023Article
- Tumor-associated macrophages mediate resistance of EGFR-TKIs in non-small cell lung cancer: mechanisms and prospects.Frontiers in immunology · 2023Review
- MicroRNAs and Drug Resistance in Non-Small Cell Lung Cancer: Where Are We Now and Where Are We Going.Cancers · 2022Review
- Review
- Article
- Cosuppression of NF-κB and AICDA Overcomes Acquired EGFR-TKI Resistance in Non-Small Cell Lung Cancer.Cancers · 2022Article
- Overview on Molecular Biomarkers for Laryngeal Cancer: Looking for New Answers to an Old Problem.Cancers · 2022Review
- MicroRNAs as the critical regulators of tyrosine kinase inhibitors resistance in lung tumor cells.Cell communication and signaling : CCS · 2022Review
- MiR-206 suppresses the deterioration of intrahepatic cholangiocarcinoma and promotes sensitivity to chemotherapy by inhibiting interactions with stromal CAFs.International journal of biological sciences · 2022Article
- STAT3 inhibitor BBI608 enhances the antitumor effect of gefitinib on EGFR-mutated non-small cell lung cancer cells.Human cell · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistently activated IL-6/STAT3 pathway promotes acquired resistance to targeted therapy with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) in non-small-cell lung cancer (NSCLC) treatment. miR-206 has been verified to be dysregulated and plays as a negative regulator in lung cancer. However, whether miR-206 may overcome IL6-induced gefitinib resistance in EGFR-mutant lung cancer remains elusive. In this study, we investigated the role of miR-206 in IL6-induced gefitinib-resistant EGFR-mutated lung cancer cell lines. We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway. Specifically, mechanistic investigations revealed that miR-206 blocked IL-6/STAT3 signalling via directly targeting the 3'-UTR of intracellular IL-6 messenger RNA. Moreover, IL-6 induced miR-206 down-regulation by reducing the cropping process of primary miR-206 (pri-miR-206) into the Drosha/DGCR8 complex. Taken together, our findings reveal a direct role of miR-206 in regulating IL-6/STAT3 pathway and contrarily activated IL-6/STAT3 signalling mediates the miR-206 maturation process in gefitinib-resistant EGFR-mutant lung cancer cells.
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