ArticleJournal of molecular cell biology2025
ENO1-BACE2-mediated LDLR cleavage promotes liver cancer progression by remodelling cholesterol metabolism.
Article in Journal of molecular cell 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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Who cites it
10 citing papers in PubMed.
- BACE2 Promotes Bladder Cancer Chemoresistance Through Proteolytic Activation of JAG1-Notch Signaling.Cancer innovation · 2026Article
- Elevated circulating BACE2 captures chronic glycemic burden and enhances the clinical identification of type 2 diabetes.iScience · 2026Article
- HMGCS1 drives cholesterol-dependent membrane repair and shields tumor cells from lymphocyte attack.Nature communications · 2026Article
- Gender differences in the plasma profiles of proprotein convertase subtilisin/kexin-type 9 (PCSK9), soluble low-density lipoprotein receptor (sLDLR), total cholesterol, and triglycerides in patients with colorectal cancer liver metastases: diagnostic and prognostic implications.Lipids in health and disease · 2026Article
- ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.International journal of molecular sciences · 2026Review
- Article
- BACE2 tunes lipid uptake through lipid transporters shedding supporting cancer cell proliferation.Journal of experimental & clinical cancer research : CR · 2026Article
- Cholesterol metabolic rewiring shapes immune remodeling across hepatocarcinogenesis.Frontiers in immunology · 2026Review
- GUDCA drives colorectal cancer progression via ALKBH5-mediated m6A modification of ENO1 and glycolytic reprogramming.Frontiers in pharmacology · 2026Article
- A chemokine-based prognostic model featuring CXCL8, ITGA5, BACE2, CCR7, CERS4, and MEI1 for cervical cancer.European journal of medical research · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Enolase 1 (ENO1) is a glycolytic enzyme involved in tumour progression that performs a variety of classical and nonclassical functions. However, the mechanism by which it promotes tumour progression is still not fully understood. Here, we found that ENO1 can bind to β-site amyloid precursor protein cleaving enzyme 2 (BACE2), a codependent gene of ENO1, in liver cancer cells. By suppressing lysosomal-dependent degradation, ENO1 stabilizes BACE2 protein level without affecting its messenger RNA level. Further analysis revealed that ENO1 and BACE2 promote low-density lipoprotein receptor (LDLR) cleavage, leading to decreased absorption of exogenous cholesterol. To maintain intracellular cholesterol levels, ENO1 and BACE2 upregulate the expression of genes involved in de novo cholesterol synthesis through a negative feedback mechanism. Both in vitro and in vivo, BACE2 mediates the tumour-promoting effect of ENO1 in liver cancer. Finally, high expression levels of ENO1 and BACE2 and low expression levels of LDLR were detected in clinical hepatocellular carcinoma samples, and abnormal expression of the ENO1-BACE2-LDLR axis was significantly associated with poor prognosis in patients with liver cancer. These data collectively demonstrated that ENO1 functions in protein cleavage by binding to BACE2 and promotes liver cancer progression by reprogramming cholesterol metabolism.
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