ArticleOncotarget2017
HMGB1 promotes myeloid-derived suppressor cells and renal cell carcinoma immune escape.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Macrophage Response to Avirulent and Virulent Mycobacterium tuberculosis and Anti-TB Effects of Exosome Treatment.Genomics, proteomics & bioinformatics · 2025Article
- Mechanism of action of HMGB1 in urologic malignancies.Frontiers in oncology · 2025Review
- The lymphocyte-to-monocyte ratio as a significant inflammatory marker associated with survival of patients with metastatic renal cell carcinoma treated using nivolumab plus ipilimumab therapy.International journal of clinical oncology · 2024Article
- Article
- Optimal timing and sequence of combining stereotactic radiosurgery with immune checkpoint inhibitors in treating brain metastases: clinical evidence and mechanistic basis.Journal of translational medicine · 2023Review
- Review
- Enhancing immune checkpoint blockade therapy of genitourinary malignancies by co-targeting PMN-MDSCs.Biochimica et biophysica acta. Reviews on cancer · 2022Article
- Peritumoral B cells drive proangiogenic responses in HMGB1-enriched esophageal squamous cell carcinoma.Angiogenesis · 2022Article
- The HMGB1 (C106A) mutation inhibits IL-10-producing CD19Frontiers in immunology · 2022Article
- Extracellular HMGB1 interacts with RAGE and promotes chemoresistance in acute leukemia cells.Cancer cell international · 2021Article
- Review
- Evaluation of autophagy mediators in myeloid-derived suppressor cells during human tuberculosis.Cellular immunology · 2021Article
- HN1L promotes migration and invasion of breast cancer by up-regulating the expression of HMGB1.Journal of cellular and molecular medicine · 2021Article
- Characterization of Molecular Heterogeneity Associated With Tumor Microenvironment in Clear Cell Renal Cell Carcinoma to Aid Immunotherapy.Frontiers in cell and developmental biology · 2021Article
- High Mobility Group Box 1 in Human Cancer.Cells · 2020Review
- RCC Immune Microenvironment Subsequent to Targeted Therapy: A Friend or a Foe?Frontiers in oncology · 2020Review
- HMGB1 in Radiotherapy: A Two Headed Signal Regulating Tumor Radiosensitivity and Immunity.OncoTargets and therapy · 2020Review
- Roles of HMGB1 in regulating myeloid-derived suppressor cells in the tumor microenvironment.Biomarker research · 2020Review
- The Generation and Identity of Human Myeloid-Derived Suppressor Cells.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite high immunogenicity and marked presence of immune cells in the RCC(renal cell carcinoma), immunotherapy fails to develop effective anti-tumor immune responses. This is due to the negative regulatory factors in the tumor microenvironment. As the main contributor of immunosuppression, myeloid-derived suppressor cells (MDSCs) inhibited anti-tumor immunity and promoted tumor progression. Meanwhile, it is confirmed that high mobility group box-1 protein (HMGB1) shows a high expression in many solid tumors and HMGB1 with high expression is involved in tumor immune escape. However, the mechanisms linking HMGB1 with tumor immune escape are unclear. The present study aimed to explore whether HMGB1 can promote RCC immune escape by inducing the generation of MDSCs. In this study, Renca mouse model was established and the influence of HMGB1 on MDSCs was investigated by using HMGB1 antibody to downregulate the expression of HMGB1 in tumor-bearing mice. The result showed that with the down-regulation of HMGB1, the tumor growth was inhibited significantly and the mice survival was prolonged greatly. Furthermore, the differentiation and proliferation of MDSCs were inhibited both
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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.