Hypoxia-induced HMGB1/NLRP3/Caspase-1 signaling axis enhances proliferation of oral squamous cell carcinoma
Researchers have identified that the HMGB1 protein, induced by hypoxia, plays a critical role in the progression of oral squamous cell carcinoma. The study demonstrates that silencing this protein can inhibit tumor growth and improve survival outcomes in clinical and animal models.
Why it matters
This discovery provides a potential new therapeutic target for treating aggressive oral cancers by disrupting the signaling pathways that fuel tumor proliferation.
British Journal of Cancer ( 2026 ) Cite this article
The hypoxic microenvironment, a common feature of solid tumors, is critically involved in driving cancer malignancy. This research focuses on elucidating the function of high mobility group box 1 (HMGB1), induced by such hypoxia, in the context of oral squamous cell carcinoma (OSCC).
We first profiled HMGB1 expression patterns in clinical OSCC specimens and evaluated their potential associations with clinicopathological parameters. To functionally characterize HMGB1, we conducted in vitro experiments utilizing silencing strategies. The impact of chronic cyclic hypoxia and HMGB1 depletion on key cellular processes-including proliferation, pyroptosis, and cell cycle-was systematically examined in OSCC cells. Signaling activity along the HMGB1/NLRP3/Caspase-1 axis was determined by immunoblotting. Furthermore, in vivo relevance was substantiated through murine xenograft models and a 4 - NQO - induced carcinogenesis protocol.
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