ArticlePloS one2012
STAT3 is activated by JAK2 independent of key oncogenic driver mutations in non-small cell lung carcinoma.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 122 citations in OpenAlex.
- A phase 1b study of erlotinib and momelotinib for the treatment of EGFR-mutated, tyrosine kinase inhibitor-naive metastatic non-small cell lung cancer.Cancer chemotherapy and pharmacology · 2022Trial
- IL‑6: A key player in the EGFR‑TKI‑resistant tumor microenvironment and its therapeutic implications (Review).International journal of oncology · 2026Review
- NCES: A Cell-Specific Network-Augmented Essentiality Framework for Cancer Therapeutic Target Discovery.Computational and structural biotechnology journal · 2026Article
- Overexpression of IL-6 and STAT3 may provide new insights into ovine pulmonary adenocarcinoma development.BMC veterinary research · 2025Article
- Genomic trajectories of colorectal cancer with choroidal metastasis: longitudinal insights from tissue and liquid biopsy via next-generation sequencing.Frontiers in genetics · 2025Article
- Acquired immunity mechanisms in sheep infected withFrontiers in veterinary science · 2025Article
- Selective inhibition of canonical STAT3 signaling suppresses K-ras mutant lung tumorigenesis and reinvigorates anti-tumor immunity.Frontiers in immunology · 2025Article
- The Streptococcus virulence protein PepO triggers anti-tumor immune responses by reprograming tumor-associated macrophages in a mouse triple negative breast cancer model.Cell & bioscience · 2023Article
- Molecular mechanism of Rhubarb in the treatment of non-small cell lung cancer based on network pharmacology and molecular docking technology.Molecular diversity · 2023Article
- Article
- Targeting Inflammation in Non-Small Cell Lung Cancer through Drug Repurposing.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Cell Type-Specific Roles of STAT3 Signaling in the Pathogenesis and Progression of K-ras Mutant Lung Adenocarcinoma.Cancers · 2022Review
- The role of IL-6/JAK2/STAT3 signaling pathway in cancers.Frontiers in oncology · 2022Review
- Role of JAK2/STAT3 Signaling Pathway in the Tumorigenesis, Chemotherapy Resistance, and Treatment of Solid Tumors: A Systemic Review.Journal of inflammation research · 2022Review
- Immunoregulatory mechanism studies of ginseng leaves on lung cancer based on network pharmacology and molecular docking.Scientific reports · 2021Article
- Transient prenatal ruxolitinib treatment suppresses astrogenesis during development and improves learning and memory in adult mice.Scientific reports · 2021Article
- Chronic exposure to methylmercury enhances the anorexigenic effects of leptin in C57BL/6J male mice.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Article
- Leptin Receptor Overlapping Transcript (LEPROT) Is Associated with the Tumor Microenvironment and a Prognostic Predictor in Pan-Cancer.Frontiers in genetics · 2021Article
- The Role of Tumor Inflammatory Microenvironment in Lung Cancer.Frontiers in pharmacology · 2021Review
- Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive activation of STAT3 is a common feature in many solid tumors including non-small cell lung carcinoma (NSCLC). While activation of STAT3 is commonly achieved by somatic mutations to JAK2 in hematologic malignancies, similar mutations are not often found in solid tumors. Previous work has instead suggested that STAT3 activation in solid tumors is more commonly induced by hyperactive growth factor receptors or autocrine cytokine signaling. The interplay between STAT3 activation and other well-characterized oncogenic "driver" mutations in NSCLC has not been fully characterized, though constitutive STAT3 activation has been proposed to play an important role in resistance to various small-molecule therapies that target these oncogenes. In this study we demonstrate that STAT3 is constitutively activated in human NSCLC samples and in a variety of NSCLC lines independent of activating KRAS or tyrosine kinase mutations. We further show that genetic or pharmacologic inhibition of the gp130/JAK2 signaling pathway disrupts activation of STAT3. Interestingly, treatment of NSCLC cells with the JAK1/2 inhibitor ruxolitinib has no effect on cell proliferation and viability in two-dimensional culture, but inhibits growth in soft agar and xenograft assays. These data demonstrate that JAK2/STAT3 signaling operates independent of known driver mutations in NSCLC and plays critical roles in tumor cell behavior that may not be effectively inhibited by drugs that selectively target these driver mutations.
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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.