ArticleMedical oncology (Northwood, London, England)2022
Knockout of high-mobility group box 1 in B16F10 melanoma cells induced host immunity-mediated suppression of in vivo tumor growth.
Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of functional murine mitochondrial formyl peptides and their effects on myeloid-derived suppressor cell generation.FEBS open bio · 2026Article
- Tumor-derived mitochondrial formyl peptides suppress tumor immunity through modification of the tumor microenvironment.Cancer science · 2024Article
- IFN-γ lowers tumor growth by increasing glycolysis and lactate production in a nitric oxide-dependent manner: implications for cancer immunotherapy.Frontiers in immunology · 2023Article
- Suppression of high mobility group box 1 in B16F10 tumor does not inhibit the induction of neoantigen-specific T cells.Cancer science · 2022Article
- Role of HMGB1 in Cutaneous Melanoma: State of the Art.International journal of molecular sciences · 2022Review
- Yiqi Jianpi Kangai Decoction Enhances the Chemotherapy Effect by Inducing Apoptosis and Regulating Treg and Th17 Cells in Colorectal Cancer Mice Model with Spleen Qi Deficiency.Journal of evidence-based integrative medicineArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
High-mobility group box 1 (HMGB1) has been reported as a damage-associated molecular pattern (DAMP) molecule that is released from damaged or dead cells and induces inflammation and subsequent innate immunity. However, the role of HMGB1 in the anti-tumor immunity is unclear since inflammation in the tumor microenvironment also contributes to tumor promotion and progression. In the present study, we established HMGB1-knockout clones from B16F10 and CT26 murine tumors by genome editing using the CRISPR/Cas9 system and investigated the role of HMGB1 in anti-tumor immunity. We found that (1) knockout of HMGB1 in the tumor cells suppressed in vivo, but not in vitro, tumor growth, (2) the suppression of the in vivo tumor growth was mediated by CD8 T cells, and (3) infiltration of CD8 T cells, macrophages and dendritic cells into the tumor tissues was accelerated in HMGB1-knockout tumors. These results demonstrated that knockout of HMGB1 in tumor cells converted tumors from poor infiltration of immune cells called "cold" to "immune-inflamed" or "hot" and inhibited in vivo tumor growth mediated by cytotoxic T lymphocytes. Infiltration of immune cells to the tumor microenvironment is an important step in the series known as the cancer immunity cycle. Thus, manipulation of tumor-derived HMGB1 might be applicable to improve the clinical outcomes of cancer immunotherapies, including immune checkpoint blockades and cancer vaccine therapies.
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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.