Background
Aerobic 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.
Conclusion
The 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.
Methods
The 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.
Results
FXR 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.