ArticleInternational journal of molecular medicine2020
The JAK2/STAT3 pathway inhibitor, AG490, suppresses the abnormal behavior of keloid fibroblasts in vitro.
Article in International journal of molecular medicine, 2020. 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, 54 citations in OpenAlex.
- Differential responses to folic acid in an established keloid fibroblast cell line are mediated by JAK1/2 and STAT3.PloS one · 2021Trial
- Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway.International journal of molecular sciences · 2026Review
- SETD2 inhibited T-cell acute lymphocytic leukemia invasion and infiltration by inhibiting the JAK/STAT pathway.Molecular and cellular biochemistry · 2026Article
- Leptin Drives Breast Cancer Aggressiveness Acting Through the Activation of the NCOA1/STAT3 Pathway.Medical sciences (Basel, Switzerland) · 2026Article
- Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway.Recent patents on anti-cancer drug discovery · 2026Article
- Mesenchymal stem cells attenuate keloid pathogenesis via TGF-β1/SMAD-driven MMP9 suppression: mechanistic insights into collagen remodeling and extracellular matrix homeostasis.Blood science (Baltimore, Md.) · 2025Article
- Post-translational modifications of collagen and its related diseases in metabolic pathways.Acta pharmaceutica Sinica. B · 2025Review
- The regulatory role of immune microenvironment-related cells and pathways in the pathogenesis of keloids.Frontiers in immunology · 2025Review
- Botulinum toxin type A inhibits the formation of hypertrophic scar through the JAK2/STAT3 pathway.Biomolecules & biomedicine · 2024Article
- Periostin regulates the activity of keloid fibroblasts by activating the JAK/STAT signaling pathway.Heliyon · 2024Article
- Article
- Comprehensive Insights into Keloid Pathogenesis and Advanced Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Small Molecule Tyrosine Kinase Inhibitors (TKIs) for Glioblastoma Treatment.International journal of molecular sciences · 2024Review
- Roles of MMP-2 and MMP-9 and their associated molecules in the pathogenesis of keloids: a comprehensive review.Frontiers in pharmacology · 2024Review
- Mechanism of piR-1245/PIWI-like protein-2 regulating Janus kinase-2/signal transducer and activator of transcription-3/vascular endothelial growth factor signaling pathway in retinal neovascularization.Neural regeneration research · 2023Article
- Diagnosis and Treatment of Keloid: Method Summary and Effect Evaluation.Clinical, cosmetic and investigational dermatology · 2023Review
- Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway.Acta cirurgica brasileira · 2023Article
- An updated review of the immunological mechanisms of keloid scars.Frontiers in immunology · 2023Review
- Oral squamous cell carcinoma cell-derived GM-CSF regulates PD-L1 expression in tumor-associated macrophages through the JAK2/STAT3 signaling pathway.American journal of cancer research · 2023Article
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AG490 is a selective inhibitor of the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. The present study examined its effects on the abnormal behavior of human keloid fibroblasts (HKFs) and evaluated its potential use in the treatment of keloids. Human normal fibroblasts (HNFs) and HKFs were treated with increasing concentrations of AG490. The proliferation of HNFs and HKFs was inhibited by AG490 in both a time‑ and concentration‑dependent manner by increasing apoptosis and inducing G1 cell cycle arrest. The downregulation of cyclin D1 and connective tissue growth factor (CTGF) expression was associated with a decrease in STAT3 expression in response to AG490. The effects of AG490 on TGF‑β‑stimulated fibroblasts, including HNFs, HKFs and hypertrophic scar fibroblasts (HSFs) were also evaluated. The TGF‑β1‑stimulated excessive proliferation and CTGF production were markedly inhibited by the application of AG490 in the HNFs, HSFs and HKFs. In addition, the STAT3‑specific decoy oligodeoxynucleotides (SODNs) were transfected into HKFs. The invasive ability of the SODN‑transfected HKFs was determined and the expression of extracellular matrix components was quantified. Similarly, SODNs blocked the constitutive activation of STAT3. SODNs inhibited the invasion and progression of HKFs, possibly via the upregulation of the expression of tissue inhibitor of metalloproteinase‑2 (TIMP‑2), and the downregulation of the expression of matrix metalloproteinase‑2 (MMP‑2) and vascular endothelial growth factor (VEGF). On the whole, the findings of the present study demonstrate that STAT3‑specific elimination, such as the application of AG490 and decoy ODNs, may serve as promising therapeutic strategies for the treatment of keloids.
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