ArticleNature communications2024
The transcription factor ChREBP Orchestrates liver carcinogenesis by coordinating the PI3K/AKT signaling and cancer metabolism.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 43 citations in OpenAlex.
- Matrine Suppresses Lung Cancer Progression via Dual Inhibition of CHEK1-Mediated DNA Damage Repair and PI3K/AKT Survival Signaling.Thoracic cancer · 2026Article
- Sugar Shockwaves: How the Fructose-Glucose-ChREBP Pathway Hijacks Liver Metabolism.Life (Basel, Switzerland) · 2026Review
- CNOT9 affects hepatocellular carcinoma proliferation and cell cycle through the PTEN/AKT/p53 signaling pathway.Human cell · 2026Article
- Targeting the LY6H-PI3K/AKT autophagy axis suppresses HCC malignancy and reveals a druggable vulnerability.Cell death & disease · 2026Article
- Carbohydrate responsive element binding protein promotes colorectal carcinogenesis via Wnt/β-catenin pathway.Oncogene · 2026Article
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- Epigenetic regulation in a high-sugar environment (Review).International journal of molecular medicine · 2026Review
- Targeted Therapy and Immunotherapies in Hepatocellular Carcinoma: Mechanisms and Clinical Studies.MedComm · 2026Review
- Long non-coding RNA (lncRNA)Translational cancer research · 2026Article
- Article
- Acetyl-coenzyme A synthetase 2-mediated acetyl-coenzyme A accumulation promotes mitophagy and tumor growth via increased H3K27ac in hepatitis B virus-related hepatocellular carcinoma.Clinical and molecular hepatology · 2026Article
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- RBBP6 and cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- Does consumption of a high-fructose diet during pregnancy and lactation exacerbate the effects of maternal exposure to cadmium on development and metabolic function of mouse offspring?Journal of toxicology and environmental health. Part A · 2026Article
- Unraveling the role of ChREBP in lung adenocarcinoma: Expression, regulatory networks, and potential functional impact.PloS one · 2026Article
- Comparative proteomic analysis of colorectal cancer stem cells reveals potential biomarkers and altered pathways.Frontiers in molecular biosciences · 2026Article
- ChREBPα: a central metabolic sensor driving lipid droplet renewal in preimplantation mouse embryos.Frontiers in cell and developmental biology · 2026Article
- Ultra-small coordination dihydromyricetin nanodots attenuate alveolar bone resorption in periodontitis through inhibition of ITGB3-Driven osteoclast differentiation.Materials today. Bio · 2025Article
- Molecular network of metabolic reprogramming and precision diagnosis and treatment of hepatocellular carcinoma.Biomarker research · 2025Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer cells integrate multiple biosynthetic demands to drive unrestricted proliferation. How these cellular processes crosstalk to fuel cancer cell growth is still not fully understood. Here, we uncover the mechanisms by which the transcription factor Carbohydrate responsive element binding protein (ChREBP) functions as an oncogene during hepatocellular carcinoma (HCC) development. Mechanistically, ChREBP triggers the expression of the PI3K regulatory subunit p85α, to sustain the activity of the pro-oncogenic PI3K/AKT signaling pathway in HCC. In parallel, increased ChREBP activity reroutes glucose and glutamine metabolic fluxes into fatty acid and nucleic acid synthesis to support PI3K/AKT-mediated HCC growth. Thus, HCC cells have a ChREBP-driven circuitry that ensures balanced coordination between PI3K/AKT signaling and appropriate cell anabolism to support HCC development. Finally, pharmacological inhibition of ChREBP by SBI-993 significantly suppresses in vivo HCC tumor growth. Overall, we show that targeting ChREBP with specific inhibitors provides an attractive therapeutic window for HCC treatment.
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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.