ArticleJournal of orthopaedic surgery and research2026
LncRNA GAS5 inhibits the remodeling of the tumor microenvironment by binding to miR-93-5p, thereby suppressing the development of osteosarcoma.
Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The inflammatory tumor immune microenvironment is being increasingly recognized as a key driver of osteosarcoma (OS) progression; however, the molecular mechanisms linking long noncoding RNAs (lncRNAs) to inflammasome signaling in OS remain poorly understood. In this study, we investigated the role of growth arrest-specific transcript 5 (GAS5) in regulating inflammatory remodeling and tumor development. We found that GAS5 expression was significantly decreased in osteosarcoma cells, whereas miR-93-5p expression was upregulated, indicating a potential inverse regulatory relationship. Mechanistically, GAS5 functioned as a competing endogenous RNA for miR-93-5p, thereby alleviating miR-93-5p-mediated downregulation of the E3 ubiquitin ligase TRIM31. Restoration of TRIM31 expression promoted NLRP3 protein turnover and attenuated inflammasome activation, as evidenced by reduced cleaved caspase-1, GSDMD-N, and IL-18 secretion. Functionally, GAS5 overexpression suppressed inflammatory cytokine production and limited protumorigenic inflammatory remodeling, ultimately inhibiting osteosarcoma cell progression. Collectively, our findings reveal a novel GAS5/miR-93-5p/TRIM31/NLRP3 regulatory axis that connects lncRNA-mediated posttranscriptional control to inflammasome signaling in osteosarcoma, providing new mechanistic insight and a potential therapeutic framework for targeting inflammation-associated OS progression.
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