As we commemorate World Cancer Day, it’s crucial to spotlight groundbreaking researches that drive our path to discovery cancer mechanism.
Among these researches, High Mobility Group Box 1 (HMGB1) and its dual role in tumor immunity has emerged as a pivotal player in the complex interplay of tumor immunity, demonstrating a dual role in understanding its potential as target in cancer immunotherapy.
HMGB1, a non-histone protein highly present in mammalian cell nuclei, emerges in fact as both a foe and ally within the cancer battlefield, underlineing one more time the complexity of our immune system’s interaction with cancer.
Immunosuppressive Effects: High Mobility Group Box 1 intricately modulates the tumor microenvironment by fostering the proliferation and survival of myeloid-derived suppressor cells (MDSCs), aiding in the differentiation and activation of regulatory T cells (Tregs), and promoting the recruitment and polarization of tumor-associated macrophages (TAMs). These actions contribute to tumor immune escape and suppression of antitumor immunity.
Immunoenhancing Effects: conversely, HMGB1 is instrumental in orchestrating immunogenic cell death (ICD), a critical mechanism in anticancer therapies. Through its release during cell death, HMGB1 signals danger to the immune system, helping the activation and recruitment of antigen-presenting cells and thereby enhancing the cytotoxic T lymphocyte response against tumor cells.
Understanding the real mechanisms of HMGB1 action, including its secretion pathways, the impact of post-translational modifications, and its interaction with cellular receptors, is paramount. Addressing these aspects could unlock new therapeutic strategies, turning HMGB1 into a targetable asset in the fight against cancer.
The goal is not only to counteract its immunosuppressive effects but also to harness its immunoenhancing capabilities, aiming for a balanced approach in cancer treatment.
HMGBiotech Srl can provide comprehensive information to facilitate informed decision-making for research involving HMGB1.
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Read the full article about the study: https://pubmed.ncbi.nlm.nih.gov/37919057
