ArticleActa pharmacologica Sinica2026
Targeting USP8 with odoroside A regulates LXRβ-mediated fatty acid metabolic reprogramming against colorectal cancer.
Article in Acta pharmacologica Sinica, 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
Colorectal cancer (CRC) remains a significant global health challenge, characterized by high post-surgical recurrence and poor survival outcomes. This study explores the therapeutic potential of odoroside A (OA), a natural compound derived from Nerium oleander, focusing on its ability to modulate lipid metabolism and induce cancer cell death on CRC. In a subcutaneous xenograft tumor model with HT29 and RKO cells, OA achieved inhibition ratios of 81.07% and 78.26% at a dose of 1.5 mg/kg, respectively. Mechanistic insights revealed that OA induced lipid accumulation and triggered cell death through lipid peroxidation, primarily by inhibiting fatty acid oxidation (FAO) pathways. This effect was supported by decreased mitochondrial FAO activity and reduced expression of FAO-related proteins, including CPT1A, CPT1B, CPT1C, CPT2, and ACSL1. Additionally, OA targeted ubiquitin-specific peptidase 8 (USP8), promoting the ubiquitination and degradation of liver X receptor beta (LXRβ), a critical regulator of lipid metabolism. This downregulation of LXRβ further disrupted FAO. This study establishes a foundation for developing OA as a natural compound-based anticancer therapy for CRC and identifies a novel link between USP8 and LXRβ, offering new insights into lipid metabolism on CRC.
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