ArticleMolecular cancer therapeutics2015
Targeted Blockade of JAK/STAT3 Signaling Inhibits Ovarian Carcinoma Growth.
Article in Molecular cancer therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 90 citations in OpenAlex.
- Phase I and Randomized Phase II Study of Ruxolitinib With Frontline Neoadjuvant Therapy in Advanced Ovarian Cancer: An NRG Oncology Group Study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Trial
- Discovery of Natural Compound α-Hederin via Large-Scale Screening as a Targeted JAK/STAT3 Inhibitor for Ovarian Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dual role of miR-155 and exosomal miR-155 in tumor angiogenesis: implications for cancer progression and therapy.European journal of medical research · 2025Review
- Evaluation of the In Vivo Efficacy of the JAK Inhibitor AZD1480 in Uterine Leiomyomas Using a Patient-derived Xenograft Murine Model.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Integrated multi-omics analysis reveals the immunotherapeutic significance of tumor cells with high FN1 expression in ovarian cancer.Frontiers in molecular biosciences · 2025Article
- Exosomes released by oxidative stress-induced mesenchymal stem cells promote murine mammary tumor progression through activating the STAT3 signaling pathway.Molecular and cellular biochemistry · 2024Article
- Applications of Innovation Technologies for Personalized Cancer Medicine: Stem Cells and Gene-Editing Tools.ACS pharmacology & translational science · 2023Review
- Mitophagy genes in ovarian cancer: a comprehensive analysis for improved immunotherapy.Discover oncology · 2023Article
- The extracellular vesicles targeting tumor microenvironment: a promising therapeutic strategy for melanoma.Frontiers in immunology · 2023Review
- Selective suppression of melanoma lacking IFN-γ pathway by JAK inhibition depends on T cells and host TNF signaling.Nature communications · 2022Article
- Article
- Applications of Proteomics in Ovarian Cancer: Dawn of a New Era.Proteomes · 2022Review
- Curcumol Attenuates Endometriosis by Inhibiting the JAK2/STAT3 Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Review
- TRIM47 promotes ovarian cancer cell proliferation, migration, and invasion by activating STAT3 signaling.Clinics (Sao Paulo, Brazil) · 2022Article
- NR1D1 suppressed the growth of ovarian cancer by abrogating the JAK/STAT3 signaling pathway.BMC cancer · 2021Article
- Triptolide inhibits JAK2/STAT3 signaling and induces lethal autophagy through ROS generation in cisplatin‑resistant SKOV3/DDP ovarian cancer cells.Oncology reports · 2021Article
- Combined inhibition of Ref-1 and STAT3 leads to synergistic tumour inhibition in multiple cancers using 3D and in vivo tumour co-culture models.Journal of cellular and molecular medicine · 2021Article
- Analysis of Autophagy-Related Signatures Identified Two Distinct Subtypes for Evaluating the Tumor Immune Microenvironment and Predicting Prognosis in Ovarian Cancer.Frontiers in oncology · 2021Article
- Combined inhibition of JAK1/2 and DNMT1 by newly identified small-molecule compounds synergistically suppresses the survival and proliferation of cervical cancer cells.Cell death & disease · 2020Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Ovarian carcinoma is the fifth leading cause of death among women in the United States. Persistent activation of STAT3 is frequently detected in ovarian carcinoma. STAT3 is activated by Janus family kinases (JAK) via cytokine receptors, growth factor receptor, and non-growth factor receptor tyrosine kinases. Activation of STAT3 mediates tumor cell proliferation, survival, motility, invasion, and angiogenesis, and recent work demonstrates that STAT3 activation suppresses antitumor immune responses and supports tumor-promoting inflammation. We hypothesized that therapeutic targeting of the JAK/STAT3 pathway would inhibit tumor growth by direct effects on ovarian carcinoma cells and by inhibition of cells in the tumor microenvironment (TME). To test this, we evaluated the effects of a small-molecule JAK inhibitor, AZD1480, on cell viability, apoptosis, proliferation, migration, and adhesion of ovarian carcinoma cells in vitro. We then evaluated the effects of AZD1480 on in vivo tumor growth and progression, gene expression, tumor-associated matrix metalloproteinase (MMP) activity, and immune cell populations in a transgenic mouse model of ovarian carcinoma. AZD1480 treatment inhibited STAT3 phosphorylation and DNA binding, and migration and adhesion of cultured ovarian carcinoma cells and ovarian tumor growth rate, volume, and ascites production in mice. In addition, drug treatment led to altered gene expression, decreased tumor-associated MMP activity, and fewer suppressor T cells in the peritoneal TME of tumor-bearing mice than control mice. Taken together, our results show pharmacologic inhibition of the JAK2/STAT3 pathway leads to disruption of functions essential for ovarian tumor growth and progression and represents a promising therapeutic strategy.
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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.