ReviewJournal of advanced research2026
Research progress and therapeutic strategies in hepatocellular carcinoma metabolic reprogramming.
Review in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- USP4-Dependent CHAF1B Stabilization Regulates Distinct SETDB1 Ubiquitin States Linked to AKT T308 Signaling and Lipogenic Remodeling in HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of the CYP19A1-GPER1 axis as a critical oncogenic driver in hepatocellular carcinoma via AKT activation.Journal of translational medicine · 2026Article
- MTARC1 p.A165 ablation reduces hepatocellular carcinoma aggressiveness in vitro and in vivo.Clinical and molecular hepatology · 2026Article
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Single-cell RNA sequencing and spatial transcriptomic analysis reveal a distinct population of G6PDFrontiers in immunology · 2026Article
- ANP32A interacts with LDHA to modulate glycolysis and ferroptosis in hepatocellular carcinoma.Frontiers in oncology · 2026Article
- A Prognostic Risk Model for Hepatocellular Carcinoma Integrating Ferroptosis and Metabolic Reprogramming Signatures.Journal of Cancer · 2026Article
- DCUN1D5 as a New Biomarker and Regulator of Fatty Acid Metabolism in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Article
- The role of USP19 in human diseases: from molecular function to clinical relevance.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with therapeutic resistance posing a significant clinical challenge. Metabolic reprogramming, a hallmark of cancer, enables tumor cells to alter metabolic pathways to meet their increased energy and biosynthetic demands, playing a critical role in HCC initiation, progression, and drug resistance. AIM OF REVIEW: This review aims to elucidate the mechanisms underlying metabolic alterations in HCC, including fatty acid, protein, and amino acid metabolism, and to explore their implications in tumor progression and therapeutic resistance. Additionally, it highlights emerging therapeutic strategies targeting key enzymes in metabolic pathways for HCC. KEY SCIENTIFIC CONCEPTS OF REVIEW: Metabolism reprogramming is closely associated with HCC proliferation and metastasis, while the interplay between metabolic pathways further drives disease progression. Targeting key metabolic enzymes and pathways through combination therapies and novel drug development shows promising clinical potential. This review provides a comprehensive analysis of metabolic reprogramming in HCC and underscores the importance of understanding these mechanisms to develop more effective therapeutic interventions.
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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 OpenQuestion graph.