ArticleJournal of clinical laboratory analysis2022
CEBPB regulates the bile acid receptor FXR to accelerate colon cancer progression by modulating aerobic glycolysis.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 19 citations in OpenAlex.
- Multi-omics Approaches to CCAAT/Enhancer-Binding Protein Beta in Oral Squamous Cell Carcinoma: Crosstalk Between Tumor Cells and Tumor-Associated Macrophages Driving Disease Progression.Current cancer drug targets · 2026Article
- Article
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Phytochemical profiling and anticancer potential of pistachio wastes against MCF-7 breast cancer cells: a metabolic and apoptotic pathway analysis.BMC complementary medicine and therapies · 2025Article
- Crosstalk Between Bile Acids and Intestinal Epithelium: Multidimensional Roles of Farnesoid X Receptor and Takeda G Protein Receptor 5.International journal of molecular sciences · 2025Review
- Emerging role of bile acids in colorectal liver metastasis: From molecular mechanism to clinical significance (Review).International journal of oncology · 2025Review
- C/EBPβ-Lin28a positive feedback loop triggered by C/EBPβ hypomethylation enhances the proliferation and migration of vascular smooth muscle cells in restenosis.Chinese medical journal · 2025Article
- Design and Evaluation of RNA Aptamer-Mediated Delivery of C/EBPJournal of nucleic acids · 2025Article
- A Narrative Review: Immunometabolic Interactions of Host-Gut Microbiota and Botanical Active Ingredients in Gastrointestinal Cancers.International journal of molecular sciences · 2024Review
- DPEP Inhibits Cancer Cell Glucose Uptake, Glycolysis and Survival by Upregulating Tumor Suppressor TXNIP.Cells · 2024Article
- Itraconazole inhibits tumor growth via CEBPB-mediated glycolysis in colorectal cancer.Cancer science · 2024Article
- OiScience · 2024Article
- Innovative strategies to optimise colorectal cancer immunotherapy through molecular mechanism insights.Frontiers in immunology · 2024Article
- Leveraging diverse cell-death patterns to predict the prognosis, immunotherapy and drug sensitivity of clear cell renal cell carcinoma.Scientific reports · 2023Article
- Review
- CEBPB regulates the bile acid receptor FXR to accelerate colon cancer progression by modulating aerobic glycolysis.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAerobic glycolysis is a main characteristic of tumors, and inhibited glycolysis impedes the tumor development. Farnesoid X Receptor (FXR) mainly regulates bile acid metabolism. In this research, we mainly investigated whether FXR was involved in the regulation of glycolysis in colon cancer.
methodsThe differential expression analysis was performed on FXR and Enhancer Binding Protein Beta (CEBPB) data in colon cancer downloaded from The Cancer Genome Atlas (TCGA) database. Western blot and qRT-PCR were used to detect the expression levels of CEBPB and FXR. The upstream gene of FXR was predicted through bioinformatic analysis. ChIP and dual luciferease assays were performed to confirm the targeted relationship between CEBPB and FXR. Gene Set Enrichment Analysis (GSEA) was performed on FXR. Finally, the glycolysis capabilities of cells in each treatment group were detected. CCK-8, colony formation assay and flow cytometry were performed to test proliferation and apoptosis of colon cancer cells.
resultsFXR was lowly expressed at the cell level in colon cancer. In vitro assays verified the antitumor effect of FXR on colon cancer. ChIP and dual luciferase assays verified that transcription factor CEBPB bound with the promotor region of FXR, and negatively regulated the expression of FXR. Cell function assays proved that silenced expression of FXR promoted glycolysis, which promoted the development of colon cancer cells.
conclusionThe study on FXR-regulated glycolysis of colon cancer cells helps us to further understand the molecular mechanism by which FXR regulated the development of colon cancer cells.
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