ArticleOncogene2017
STAT3 activation in endothelial cells is important for tumor metastasis via increased cell adhesion molecule expression.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- Neutrophils promote endothelial cell activation in pediatric Mycoplasma pneumoniae pneumonia.JCI insight · 2026Article
- Regulatory T-cell Sensing of Extracellular ATP via P2RX7 Promotes Their Accumulation and Suppression and Drives Lung Tumor Growth.Cancer immunology research · 2026Article
- Review
- STAT3 expression is reduced in cardiac pericytes in HFpEF and its loss reduces cellular adhesion and induces pericyte senescence.FEBS letters · 2025Article
- The olfactory receptor OR51E2 regulates prostate cancer aggressiveness and modulates STAT3 in prostate cancer cells and in xenograft tumors.BMC cancer · 2025Article
- Multifaced Anticancer Potential of Doxorubicin: Spotlight on Breast Cancer.Diseases & research · 2025Article
- Uncovering the Role ofJournal of Cancer · 2025Article
- Endothelial Pim3 kinase protects the vascular barrier during lung metastasis.Nature communications · 2024Article
- The Brain Pre-Metastatic Niche: Biological and Technical Advancements.International journal of molecular sciences · 2023Review
- Single-nucleus multiregion transcriptomic analysis of brain vasculature in Alzheimer's disease.Nature neuroscience · 2023Article
- JAK-STAT inhibition reduces endothelial prothrombotic activation and leukocyte-endothelial proadhesive interactions.Journal of thrombosis and haemostasis : JTH · 2023Article
- The covert symphony: cellular and molecular accomplices in breast cancer metastasis.Frontiers in cell and developmental biology · 2023Review
- Endothelial activation and damage as a common pathological substrate in different pathologies and cell therapy complications.Frontiers in medicine · 2023Review
- miR-1246 in tumor extracellular vesicles promotes metastasisFrontiers in oncology · 2023Article
- Article
- Upcoming treatments for morphea.Immunity, inflammation and disease · 2021Review
- The Role of Bradykinin Receptors in the Etiopathogenesis of Chronic Spontaneous Urticaria.Medicina (Kaunas, Lithuania) · 2021Article
- Temporal multi-omics identifies LRG1 as a vascular niche instructor of metastasis.Science translational medicine · 2021Article
- ESDN inhibits melanoma progression by blocking E-selectin expression in endothelial cells via STAT3.Cancer letters · 2021Article
- Systematic expression analysis of the CELSR family reveals the importance of CELSR3 in human lung adenocarcinoma.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis is a life-threatening feature of cancer and is primarily responsible for cancer patient mortality. Cross talk between tumor cells and endothelium is important for tumor progression and metastasis. However, very little is known about the mechanisms by which endothelial cells (ECs) that are close to tumor cells, respond to the tumor cells during tumor progression and metastasis. In this study, we exploited the use of EC-specific signal transducer activator of transcription 3 (STAT3) knockout mice to investigate the role of STAT3 in ECs in tumor progression and metastasis. We found that the loss of STAT3 in ECs did not affect primary Lewis lung carcinoma (LLC) tumor growth, but it reduced in vivo LLC metastasis in experimental and spontaneous metastasis models. Mechanistically, STAT3 activation upregulated cell adhesion molecule expression, including E-selectin and P-selectin, in murine endothelial MS-1 cells treated with tumor cell-conditioned media in vitro and in pre-metastatic lungs of tumor-bearing mice in vivo. We also found that both E-selectin and P-selectin were, at least in part, responsible for STAT3-induced adhesion and invasion of LLC cells through an EC monolayer. However, tumor cell-conditioned media from B16F10 melanoma cells did not activate STAT3 in MS-1 cells. As a result, EC STAT3 knockout did not affect B16F10 melanoma cell metastasis. In addition, various human cancer cells activated STAT3 in human ECs (HUVECs), resulting in increased cell adhesion molecule expression. Collectively, our findings demonstrate that STAT3 activation in ECs promotes tumor metastasis through the induction of cell adhesion molecules, demonstrating a role for ECs in response to tumor cells during tumor metastasis.
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