ArticleInternational journal of cancer2009
Hypoxia induces chemoresistance in ovarian cancer cells by activation of signal transducer and activator of transcription 3.
Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 124 citations in OpenAlex.
- Patient-derived model capturing hypoxia and extracellular matrix remodelling of immunologically cold high-grade serous tumours.Nature communications · 2026Article
- Obesity-driven extracellular vesicle signaling in cancer: mechanistic insights and clinical implications.Oncogenesis · 2026Review
- Targeting G6PD with Benzimidazole and Thiazole Derivatives SuppressesInternational journal of molecular sciences · 2025Article
- Evaluating the specific STAT3 inhibitor YHO-1701 in ovarian cancer cell lines and patient-derived cell models: efficacy, mechanisms, and therapeutic potential.Journal of gynecologic oncology · 2025Article
- Multicompartmentalized Microvascularized Tumor-on-a-Chip to Study Tumor-Stroma Interactions and Drug Resistance in Ovarian Cancer.Cellular and molecular bioengineering · 2024Article
- Hypoxic Regulation of the KLK4 Gene in two Different Prostate Cancer Cells Treated with TGF- β.Cell biochemistry and biophysics · 2024Article
- CHAF1A promotes the proliferation and growth of epithelial ovarian cancer cells by affecting the phosphorylation of JAK2/STAT3 signaling pathway.Biochemistry and biophysics reports · 2023Article
- Review
- Review
- Identification of seven hypoxia-related genes signature and risk score models for predicting prognosis for ovarian cancer.Functional & integrative genomics · 2023Article
- Comparing the Secretomes of Chemorefractory and Chemoresistant Ovarian Cancer Cell Populations.Cancers · 2022Review
- The Anti-Proliferative Effect of PI3K/mTOR and ERK Inhibition in Monolayer and Three-Dimensional Ovarian Cancer Cell Models.Cancers · 2022Article
- Role of the Pro-Inflammatory Tumor Microenvironment in Extracellular Vesicle-Mediated Transfer of Therapy Resistance.Frontiers in oncology · 2022Review
- PD-L1 Regulates Inflammation in LPS-Induced Lung Epithelial Cells and Vascular Endothelial Cells by Interacting with the HIF-1α Signaling Pathway.Inflammation · 2021Article
- Characterizing Endocrine Status, Tumor Hypoxia and Immunogenicity for Therapy Success in Epithelial Ovarian Cancer.Frontiers in endocrinology · 2021Review
- Hypoxia-Mediated Decrease of Ovarian Cancer Cells Reaction to Treatment: Significance for Chemo- and Immunotherapies.International journal of molecular sciences · 2020Review
- Long non-coding RNAs in ovarian cancer: expression profile and functional spectrum.RNA biology · 2020Review
- Phosphorylation of STAT3 and ERBB2 mediates hypoxia‑induced VEGF release in ARPE‑19 cells.Molecular medicine reports · 2020Article
- Hypoxia-induced hsa_circ_0000826 is linked to liver metastasis of colorectal cancer.Journal of clinical laboratory analysis · 2020Article
- Antiangiogenesis Efficacy of Ethanol Extract fromEvidence-based complementary and alternative medicine : eCAM · 2020Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Signal transducer and activator of transcription 3 (STAT3) is activated in a variety of human cancers, including ovarian cancer. The molecular mechanism by which the STAT3 is activated in cancer cells is poorly understood. We observed that human ovarian xenograft tumors (A2780) in mice were severely hypoxic (pO(2) approximately 2 mmHg). We further observed that hypoxic exposure significantly increased the phosphorylation of STAT3 (pSTAT3) at the Tyr705 residue in A2780 cell line. The pSTAT3 (Tyr705) level was highly dependent on cellular oxygenation levels, with a significant increase at <2% O(2), and without any change in the pSTAT3 (Ser727) or total STAT3 levels. The pSTAT3 (Tyr705) elevation following hypoxic exposure could be reversed within 12 hr after returning the cells to normoxia. The increased level of pSTAT3 was partly mediated by increased levels of reactive oxygen species generation in the hypoxic cancer cells. Conventional chemotherapeutic drugs cisplatin and taxol were far less effective in eliminating the hypoxic ovarian cancer cells suggesting a role for pSTAT3 in cellular resistance to chemotherapy. Inhibition of STAT3 by AG490 followed by treatment with cisplatin or taxol resulted in a significant increase in apoptosis suggesting that hypoxia-induced STAT3 activation is responsible for chemoresistance. The results have important clinical implications for the treatment of hypoxic ovarian tumors using STAT3-specific inhibitors.
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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.