ArticleJournal of bone oncology2024
Novel lipid metabolism factor HIBCH inhibitor synergizes with doxorubicin to suppress osteosarcoma growth and impacts clinical prognosis in osteosarcoma patients.
Article in Journal of bone oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- RHBDL2 drives lipid metabolic reprogramming in osteosarcoma via USP3-mediated deubiquitination of PPT1.Cell death & disease · 2026Article
- PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis.iScience · 2025Article
- Hispidulin suppresses osteosarcoma by directly targeting FABP4 to disrupt lipid metabolism and inhibit the PI3K/AKT pathway.Journal of translational medicine · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Osteosarcoma (OS) is a highly malignant primary bone tumor primarily affecting children and adolescents. Despite advancements in therapeutic strategies, long-term survival rates for OS remain unfavorable, especially in advanced or recurrent cases. Emerging evidence has noted the involvement of lipid metabolism dysregulation in OS progression, but the specific mechanisms remain unclear. Methods: A risk model incorporating lipid metabolism-related genes was established to stratify OS patients into high-risk and low-risk groups. Functional assays were conducted to assess the role of 3-hydroxyisobutyryl-CoA hydrolase (HIBCH) in OS cell activities. Ultra-fast liquid chromatography-mass spectrometry was adopted to analyze the impact of HIBCH on OS cell metabolism. Moreover, the combined effect of HIBCH inhibitor SBF-1 with doxorubicin (DOX) was evaluated through Results: HIBCH was identified as a key gene involved in the malignant behaviors of OS cells. HIBCH knockdown disrupted tricarboxylic acid (TCA) cycle activity and reduced oxidative phosphorylation in OS cells. SBF-1 showed synergistic effects with DOX in inhibiting malignant phenotypes of OS cells by modulating the Akt-mTOR pathway. Conclusions: This study reveals the critical role of lipid metabolism in OS progression and suggests a new therapeutic strategy against chemotherapy resistance in OS based on the synergistic combination of SBF-1 with DOX.
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