ArticleGut2024
Targeting squalene epoxidase restores anti-PD-1 efficacy in metabolic dysfunction-associated steatohepatitis-induced hepatocellular carcinoma.
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Article in Gut, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46citing papers in PubMed
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Who cites it
46 citing papers in PubMed.
- Sonogenetic Control of Engineered Probiotics for the Treatment of MASH by Modulating the Gut-Liver Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- LL-37 inhibits osteosarcoma progression by suppressing SQLE-mediated cholesterol synthesis via the PTEN/AKT/mTOR pathway.Journal of bone oncology · 2026Article
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
- Pan-cancer 8q24 amplification predicts primary immunotherapy resistance and therapeutic vulnerabilities.iScience · 2026Article
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Review
- Lipid metabolism reprogramming shapes the immune landscape in the tumor microenvironment.Cellular & molecular immunology · 2026Review
- METTL16 Promotes Head and Neck Squamous Cell Carcinoma Progression via m6A-Mediated Stabilization of SREBP2 mRNA and Enhanced Cholesterol Biosynthesis.Cancer medicine · 2026Article
- Evaluation of human epidermal growth factor receptor 2 (HER2)-related genes revealed that HER2-antibody-drug conjugate (ADC) drugs confer clinical benefits to Bacillus Calmette-Guérin (BCG)-unresponsive non-muscle invasive bladder cancer patients.Translational andrology and urology · 2026Article
- Overcoming MDSC-Mediated Immunosuppression in Hepatocellular Carcinoma: From Mechanisms to Novel Immunotherapeutic Approaches.Cancers · 2026Review
- Revisiting cholesterol metabolism in hepatocellular carcinoma: a hidden driver of systemic therapy response.ESMO gastrointestinal oncology · 2026Review
- OCTN2 Activates a Non-Canonical Carnitine Metabolic Pathway to Promote MASH-HCC Progression and Immunotherapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting fatty acid metabolism for cancer therapy.Fundamental research · 2026Review
- Single-cell mapping of cholesterol metabolism reveals FDPS as a therapeutic vulnerability in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- ACLY blockade rewires tumor metabolism to boost immunity in MASH-driven hepatic cell carcinoma.Journal of the National Cancer Center · 2026Article
- From Gas Chromatography-Mass Spectrometry (GC-MS) to Network Pharmacology: System-Level Insights into the Multi-Target Biological Potential ofCurrent issues in molecular biology · 2026Article
- NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin.iScience · 2026Article
- Cholesterol metabolic rewiring shapes immune remodeling across hepatocarcinogenesis.Frontiers in immunology · 2026Review
- Targeting MDSCs in cancer: emerging immunotherapeutic and metabolic strategies.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Jun WenInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0002-6947-2087
Xiang ZhangInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0002-3222-5824
Chi Chun WongInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Yating ZhangInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Yasi PanInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Yunfei ZhouInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Alvin Ho-Kwan CheungDepartment of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong SAR, China.
Yali LiuInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Fenfen JiInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Xing KangInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Dabin LiuInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China.
Jun YuInstitute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China junyu@cuhk.edu.hk.ORCID 0000-0001-5008-2153
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveSqualene epoxidase (SQLE) promotes metabolic dysfunction-associated steatohepatitis-associated hepatocellular carcinoma (MASH-HCC), but its role in modulating the tumour immune microenvironment in MASH-HCC remains unclear.
designWe established hepatocyte-specific
resultsHepatocyte-specific
conclusionSQLE induces an impaired antitumour response in MASH-HCC via attenuating CD8
Indexed as
Carcinoma, HepatocellularLiver NeoplasmsSqualene MonooxygenaseTumor MicroenvironmentAnimalsCD8-Positive T-LymphocytesDiet, High-FatDisease Models, AnimalFatty LiverHumansImmune Checkpoint InhibitorsMiceMice, KnockoutMice, TransgenicMyeloid-Derived Suppressor CellsImmune Checkpoint InhibitorsSqualene Monooxygenasehepatobiliary cancerimmunotherapylipoprotein-cholesterolnonalcoholic steatohepatitis
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LicenceCC BY-NC
Read underepoch 390
Registered trials
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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.