ArticleRSC advances2026
A layered double hydroxide nanocarrier enables YM155 delivery-induced PANoptosis and immunogenic activation in hepatocellular carcinoma.
Article in RSC advances, 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
Hepatocellular carcinoma (HCC) remains a highly lethal malignancy due to its intrinsic resistance to apoptosis and limited response to conventional chemotherapy. This therapeutic bottleneck is closely associated with aberrant cell death regulation and an immunosuppressive tumor microenvironment, which collectively restrict effective tumor eradication. In this study, a layered double hydroxide (LDH)-based YM155 delivery platform (LDH-YM155) is developed to enhance Survivin-targeted therapy while simultaneously reprogramming tumor cell death toward an inflammatory and immunogenic phenotype. LDH-YM155 exhibits favorable physicochemical stability, pH-responsive YM155 release, and efficient cellular internalization, triggering pronounced oxidative stress and mitochondrial membrane depolarization in Hepa1-6 cells. This stress cascade activates PANoptosis characterized by elevated caspase-3, caspase-8 and caspase-1 activity, ASC speck formation, elevated p-MLKL levels, increased Annexin V/PI-positive populations, and upregulated NLRP3 and RIPK3 signaling. In parallel, LDH-YM155 induces immunogenic cell death-associated events, including enhanced calreticulin exposure, extracellular HMGB1 and ATP release, and increased lactate dehydrogenase release, thereby promoting dendritic cell maturation through tumor cell-conditioned media. Transcriptomic profiling further confirms activation of stimulus-responsive and inflammatory signaling pathways consistent with the observed phenotype.
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