ArticleCommunications biology2025
Isoacteoside alleviates hepatocellular carcinoma progression by inhibiting PDHB-mediated reprogramming of glucose metabolism.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- Citric Acid Cycle Genes and Nutrigenetics.International journal of molecular sciences · 2026Review
- Phenylethanoid Glycosides fromNutrients · 2026Review
- Metabolic reprogramming-driven resistance to multi-kinase inhibitors in hepatocellular carcinoma: molecular mechanisms and therapeutic opportunities.Molecular cancer · 2026Review
- Cuproptosis: A Potential Target for the Treatment of Systemic Lupus Erythematosus.Journal of inflammation research · 2026Review
- Integrated multi-omics profiling identifies aging-related molecular signatures and convergent interferon signaling in systemic lupus erythematosus.Frontiers in immunology · 2026Article
- miR-1343-3p regulating OGDHL/PDHB-pyruvate glucose metabolic reprogramming against gastric cancer cell proliferation.Discover oncology · 2025Article
- Molecular network of metabolic reprogramming and precision diagnosis and treatment of hepatocellular carcinoma.Biomarker research · 2025Review
- The role of dysregulated copper metabolism in diabetes and its complications: a review.Frontiers in endocrinology · 2025Review
- PKM2-driven metabolic reprogramming in digestive system tumors: mechanisms, therapeutic advances, and clinical challenges.Frontiers in immunology · 2025Review
- Copper metabolism and cuproptosis: broad perspectives in the treatment of hepatocellular carcinoma.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pyruvate dehydrogenase B (PDHB) is an important component of the pyruvate dehydrogenase complex and is implicated in altering tumor metabolism and promoting malignancy. However, the specific impact of PDHB on hepatocellular carcinoma (HCC) metabolic reprogramming and its role in tumor progression remain to be elucidated. In our investigation, we have discerned a pronounced elevation in PDHB expression within HCC, intricately linked to delayed tumor staging, heightened tumor grading, and diminished prognostic outcomes. PDHB overexpression drives tumor growth and metastasis in vitro and in vivo. Mechanistically, PDHB mediates metabolic reprogramming by binding to the promoter regions of SLC2A1, GPI, and PKM2, promoting glycolysis-related gene transcription, contributes to HCC sorafenib resistance. In addition, Isoacteoside is a targeted inhibitor of PDHB and exert antitumor effects on HCC. In the mouse xenograft model, the combination of isoacteoside and sorafenib shows significantly better effects than sorafenib alone. In summary, our study validates PDHB as an oncogenic drug resistance-related gene capable of predicting HCC tumor progression. PDHB and Isoacteoside could be potential avenues for targeted and combination therapies in liver cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.