ArticleJCI insight2017
ASK1-dependent endothelial cell activation is critical in ovarian cancer growth and metastasis.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 64 citations in OpenAlex.
- The role of tumor-associated macrophages in cancer development and their significance as prognostic markers.Clinical and experimental medicine · 2026Review
- Lactate-lactylation in tumor angiogenesis and progression: mechanisms, biomarker potential, and therapeutic implications.Biomarker research · 2026Review
- Linking tumour angiogenesis and tumour immunity.Nature reviews. Immunology · 2026Review
- FBXO22 Suppresses Oxidative Stress-Induced ASK1 Activation and Cell Death via Ubiquitination-Dependent Degradation of TRIM48.International journal of molecular sciences · 2025Article
- Role of tumor microenvironment in ovarian cancer metastasis and clinical advancements.Journal of translational medicine · 2025Review
- Obesity-associated reduction of miR-150-5p in extracellular vesicles promotes ventilator-induced lung injury by modulating the lysosomal degradation of VE-cadherin.Cell death discovery · 2025Article
- NMN Supplementation Inhibits Endothelial Cell ROS-Mediated Src/Pi3k/Akt Signaling Pathway to Protect High-Altitude Blood-Retinal Barrier.Investigative ophthalmology & visual science · 2025Article
- Beyond tumor‑associated macrophages involved in spheroid formation and dissemination: Novel insights for ovarian cancer therapy (Review).International journal of oncology · 2024Review
- ASK-1 activation exacerbates kidney dysfunction via increment of glomerular permeability and accelerates cellular aging in diabetic kidney disease model mice.Scientific reports · 2024Article
- Tumor Vasculature as an Emerging Pharmacological Target to Promote Anti-Tumor Immunity.International journal of molecular sciences · 2023Review
- Interaction of tumor‑associated macrophages with stromal and immune components in solid tumors: Research progress (Review).International journal of oncology · 2023Review
- Review
- Tumor cells-derived conditioned medium induced pro-tumoral phenotypes in macrophages through calcium-nuclear factor κB interaction.BMC cancer · 2022Article
- Apoptosis signal-regulating kinase-1 regulates thrombin-induced endothelial permeability.Vascular pharmacology · 2022Article
- Article
- Spheroid Formation and Peritoneal Metastasis in Ovarian Cancer: The Role of Stromal and Immune Components.International journal of molecular sciences · 2022Review
- A bi-directional dialog between vascular cells and monocytes/macrophages regulates tumor progression.Cancer metastasis reviews · 2021Review
- Role of lysosomes in physiological activities, diseases, and therapy.Journal of hematology & oncology · 2021Review
- ASK1 suppresses NK cell-mediated intravascular tumor cell clearance in lung metastasis.Cancer science · 2021Article
- Construction and Validation of a Macrophage-Associated Risk Model for Predicting the Prognosis of Osteosarcoma.Journal of oncology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
We have recently reported that tumor-associated macrophages (TAMs) promote early transcoelomic metastasis of ovarian cancer by facilitating TAM-ovarian cancer cell spheroid formation. ASK1 is known to be important for macrophage activation and inflammation-mediated tumorigenesis. In the present study, we show that ASK1 deficiency attenuates TAM-spheroid formation and ovarian cancer progression in an orthotopic ovarian cancer model. Interestingly, ASK1 in stroma, but not in TAMs, is critical for peritoneal tumor growth of ovarian cancer. Moreover, overexpression of an ASK1 inhibitory protein (suppressor of cytokine signaling-1; SOCS1) in vascular endothelium attenuates vascular permeability, TAM infiltration, and ovarian cancer growth. Mechanistically, we show that ASK1 mediates degradation of endothelial junction protein VE-cadherin via a lysosomal pathway to promote macrophage transmigration. Importantly, a pharmacological ASK1 inhibitor prevents tumor-induced vascular leakage, macrophage infiltration, and tumor growth in two mouse models. Since transcoelomic metastasis is also associated with many other cancers, such as pancreatic and colon cancers, our study provides ASK1 as a therapeutic target for the treatment of ovarian cancer and other transcoelomic metastasis cancers.
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Registered trials
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.