ArticleMolecular cancer therapeutics2017
JAK1/STAT3 Activation through a Proinflammatory Cytokine Pathway Leads to Resistance to Molecularly Targeted Therapy in Non-Small Cell Lung Cancer.
Article in Molecular cancer therapeutics, 2017. 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, 102 citations in OpenAlex.
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- M1C IS NECESSARY FOR DARAXONRASIB RESISTANCE OF NSCLC KRAS(G12C) MUTANT CELLS.bioRxiv : the preprint server for biology · 2026Article
- IL‑6: A key player in the EGFR‑TKI‑resistant tumor microenvironment and its therapeutic implications (Review).International journal of oncology · 2026Review
- SpatialFusion: A lightweight multimodal foundation model for pathway-informed spatial niche mapping.bioRxiv : the preprint server for biology · 2026Article
- S3RL: Enhancing Spatial Single-Cell Transcriptomics With Separable Representation Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CRISPR-Cas9 screen reveals that inhibition of enhancer of zeste homolog 2 sensitizes malignant T cells to dimethyl-fumarate-induced cell death.The FEBS journal · 2026Article
- Cancer-associated fibroblasts promote drug resistance in ALK-driven lung adenocarcinoma cells by upregulating lipid biosynthesis.Cancer & metabolism · 2025Article
- Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Cell-Specific Effects of JAK1 Inhibitors in Ulcerative Colitis.Journal of clinical medicine · 2025Review
- Editorial: Autophagy and lung cancer therapy: targeted drug development and new emerging technology.Frontiers in pharmacology · 2025Article
- Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.International journal of molecular sciences · 2024Article
- Role of the TME in immune checkpoint blockade resistance of non-small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Pan-cancer single cell and spatial transcriptomics analysis deciphers the molecular landscapes of senescence related cancer-associated fibroblasts and reveals its predictive value in neuroblastoma via integrated multi-omics analysis and machine learning.Frontiers in immunology · 2024Article
- 3D cell culture models in research: applications to lung cancer pharmacology.Frontiers in pharmacology · 2024Review
- AKAP12 promotes cancer stem cell-like phenotypes and activates STAT3 in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Oncostatin-M and OSM-Receptor Feed-Forward Activation of MAPK Induces Separable Stem-like and Mesenchymal Programs.Molecular cancer research : MCR · 2023Article
- Targeting Breast Cancer: The Familiar, the Emerging, and the Uncharted Territories.Biomolecules · 2023Review
- The role of TGF-β in the tumor microenvironment of pancreatic cancer.Genes & diseases · 2023Review
- STAT3 silencing by an aptamer-based strategy hampers the crosstalk between NSCLC cells and cancer-associated fibroblasts.Molecular therapy. Nucleic acids · 2023Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Molecularly targeted drugs have yielded significant therapeutic advances in oncogene-driven non-small cell lung cancer (NSCLC), but a majority of patients eventually develop acquired resistance. Recently, the relation between proinflammatory cytokine IL6 and resistance to targeted drugs has been reported. We investigated the functional contribution of IL6 and the other members of IL6 family proinflammatory cytokine pathway to resistance to targeted drugs in NSCLC cells. In addition, we examined the production of these cytokines by cancer cells and cancer-associated fibroblasts (CAF). We also analyzed the prognostic significance of these molecule expressions in clinical NSCLC samples. In NSCLC cells with acquired resistance to targeted drugs, we observed activation of the IL6-cytokine pathway and STAT3 along with epithelial-to-mesenchymal transition (EMT) features. In particular, IL6 family cytokine oncostatin-M (OSM) induced a switch to the EMT phenotype and protected cells from targeted drug-induced apoptosis in OSM receptors (OSMRs)/JAK1/STAT3-dependent manner. The cross-talk between NSCLC cells and CAFs also preferentially activated the OSM/STAT3 pathway via a paracrine mechanism and decreased sensitivity to targeted drugs. The selective JAK1 inhibitor filgotinib effectively suppressed STAT3 activation and OSMR expression, and cotargeting inhibition of the oncogenic pathway and JAK1 reversed resistance to targeted drugs. In the analysis of clinical samples,
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