ArticleOncogene2023
Glucose-induced and ChREBP: MLX-mediated lipogenic program promotes hepatocellular carcinoma development.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 12 citations in OpenAlex.
- New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026Review
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- Carbohydrate responsive element binding protein promotes colorectal carcinogenesis via Wnt/β-catenin pathway.Oncogene · 2026Article
- Computational analysis of multi-omics data reveals CXCL10Cellular and molecular life sciences : CMLS · 2026Article
- Rethinking the hepatoprotective potential of vegetarian diets in dysfunction-associated steatotic liver disease/metabolic-associated fatty liver disease: a critical narrative review.Frontiers in nutrition · 2026Review
- NAD + in fatty liver disease: mechanistic insights and associated targets.Cell biology and toxicology · 2025Review
- High-Resolution Quantitative Reconstruction of Microvascular Architectures in Mouse Hepatocellular Carcinoma Models.Cancers · 2025Article
- SOX4 reprograms fatty acid metabolism through the CHREBP to inhibit ferroptosis in hepatocellular carcinoma.Cell death discovery · 2025Article
- The role of fatty acid metabolism on B cells and B cell-related autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- MLX phosphorylation stabilizes the ChREBP-MLX heterotetramer on tandem E-boxes to control carbohydrate and lipid metabolism.Science advances · 2025Article
- Integration of Single-Cell and Bulk Transcriptomes to Identify a Poor Prognostic Tumor Subgroup to Predict the Prognosis of Patients with Early-stage Lung Adenocarcinoma.Journal of Cancer · 2025Article
- FUT2 promotes colorectal cancer metastasis by reprogramming fatty acid metabolism via YAP/TAZ signaling and SREBP-1.Communications biology · 2024Article
- MLX phosphorylation stabilizes the ChREBP-MLX heterotetramer on tandem E-boxes to control carbohydrate and lipid metabolism.bioRxiv : the preprint server for biology · 2024Article
- Sweet dreams could be made of this: carbohydrate-responsive element-binding protein (ChREBP) as a target for hepatocellular carcinoma therapy.Molecular oncology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Carbohydrate Response Element (ChoRE) Binding Protein (ChREBP) and its binding partner Max-like protein X (MLX) mediate transcription of lipogenic genes under glucose-rich conditions. Dysregulation of glucose and lipid metabolism frequently occurs in cancers, including Hepatocellular Carcinomas (HCCs). However, it is currently unclear whether the glucose-induced lipogenic program plays a role in the development of HCCs. Here, we show that MLX expression is elevated in HCC specimens and downregulation of MLX expression inhibits proliferation of HCC cells. In mice, liver-specific knockout of Mlx results in dramatic decrease in the expression of lipogenic genes and lipid levels in circulation. Interestingly, in the absence of Mlx, the development of tumors in multiple HCC models, such as diethylnitrosamine (DEN) treatment and hydrodynamic injection of oncogenes (AKT/RAS or CTNNB1/RAS), is robustly blocked. However, a high-fat diet can partially restore tumorigenesis in Mlx-deficient livers, indicating a critical role of lipid synthesis in HCC development. In addition, liver-specific expression of a dominant negative MLX (dnMLX) via adeno-associated virus effectively blocks tumorigenesis in mice. Thus, the glucose-induced lipogenic program is required in the development of HCC, and the ChREBP: MLX transcription factors serve as a potential target for cancer therapies.
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