ArticleAngiogenesis2022
Peritumoral B cells drive proangiogenic responses in HMGB1-enriched esophageal squamous cell carcinoma.
Article in Angiogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- HMGB1 Post-Translational Modifications in Epstein-Barr Virus-Associated Nasopharyngeal Carcinoma: Current Evidence, Emerging Mechanistic Concepts, and Unresolved Questions.International journal of molecular sciences · 2026Review
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Single-cell transcriptomics unveils pyroptosis-related immune microenvironment dynamics and prognostic modeling in esophageal squamous cell carcinoma.Journal of cardiothoracic surgery · 2026Article
- Exploratory identification of lycorine as a potential inhibitor of the ACP2/YME1L1 prognostic axis in esophageal squamous cell carcinoma: a multi-omics and computational hypothesis.Molecular genetics and genomics : MGG · 2026Article
- Intratumoural and Peritumoural Radiomics-Based Machine Learning Models for the Postoperative Survival Prediction in Oesophageal Squamous Cell Carcinoma.Interdisciplinary cardiovascular and thoracic surgery · 2026Article
- Immunosuppressive tumor microenvironment and immunotherapy resistance of esophageal carcinoma.Frontiers in immunology · 2026Review
- Construction and verification of 5-year survival prediction model for post-op ESCC patients.Frontiers in oncology · 2026Article
- Natural medicines target tumor vascular microenvironment to inhibit tumor.Genes & diseases · 2025Review
- Angiogenesis and targeted therapy in the tumour microenvironment: From basic to clinical practice.Clinical and translational medicine · 2025Review
- Review
- Alterations inContemporary oncology (Poznan, Poland) · 2025Article
- 5-O-Methylvisammioside inhibits HMGB1-induced Angiogenesis of hepatocellular carcinoma through RAGE/MEK/ERK signaling pathway.PloS one · 2025Article
- The mechanism of high mobility group box-1 protein and its bidirectional regulation in tumors.Biomolecules & biomedicine · 2024Review
- ENOX2 inhibition enhances infiltration of effector memory T-cell and mediates response to chemotherapy in immune-quiescent nasopharyngeal carcinoma.Journal of advanced research · 2024Article
- Endothelial cells in tumor microenvironment: insights and perspectives.Frontiers in immunology · 2024Review
- The multifunctional protein HMGB1: 50 years of discovery.Nature reviews. Immunology · 2023Review
- A risk prognostic model for patients with esophageal squamous cell carcinoma basing on cuproptosis and ferroptosis.Journal of cancer research and clinical oncology · 2023Article
- Exploring the crosstalk between endothelial cells, immune cells, and immune checkpoints in the tumor microenvironment: new insights and therapeutic implications.Cell death & disease · 2023Review
- Mechanisms involved in the HMGB1 modulation of tumor multidrug resistance (Review).International journal of molecular medicine · 2023Article
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several B-cell subsets with distinct functions and polarized cytokine profiles that extend beyond antibody production have been reported in different cancers. Here we have demonstrated that proliferating B cells were predominantly found in the peritumoral region of esophageal squamous cell carcinoma (ESCC). These B cells were enriched in tumor nests with high expression of high-mobility group box 1 (HMGB1). High densities of peritumoral proliferating B cells and concomitantly high intratumoral HMGB1 expression showed improved prognostic significance, surpassing prognostic stratification of ESCC patients based on HMGB1 positivity alone. This striking association led us to set up models to test whether cancer-derived HMGB1 could shape tumor microenvironment via modulation on B cells. Overexpression of HMGB1 in ESCC cell lines (KYSE510 and EC18) enhanced proliferation and migration of B cells. Transcriptomic analysis showed that migratory B cells exhibited high enrichment of proangiogenic genes. VEGF expression in proliferating B cells was induced upon co-culture of HMGB1-overexpressing tumor cells and B cells. Secretome array profiling of conditioned media (CM) from the co-culture revealed rich expression of proangiogenic proteins. Consequently, incubation of human umbilical vein endothelial cells with CM promoted angiogenesis in tube formation and migration assays. HMGB1 inhibitor, glycyrrhizin, abolishes all the observed proangiogenic phenotypes. Finally, co-injection of B cells and CM with HMGB1-overexpressing tumor cells, but not with glycyrrhizin, significantly enhanced tumor growth associated with increased microvascular density in ESCC xenograft mice model. Our results indicate that cancer-derived HMGB1 elevates angiogenesis in ESCC by shifting the balance toward proangiogenic signals in proliferating B cells.
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