Fig. 5: HMGA1 upregulates FASN in CRC.

a Differentially expressed genes in lipid metabolism in HMGA1-knockdown CRC cells compared with control CRC cells from RNA-seq. b GSEA plot of fatty acid synthesis genes identified in RNA-seq in HMGA1-silenced HT-29 cells. NES, normalized enrichment score. c Saturated and monounsaturated FFAs with ¹³C-labeled in control and HMGA1-overexpressed cells treated with orlistat. Control and HMGA1-overexpressed HT29 cells were treated with 20 µM orlistat for 18 h. Cell culture medium was then replaced with glucose free DMEM in the presence of [U-¹³C] glucose (2 g/L) and orlistat for 6 h. Each dot represents a sample (n  =  3). d The samples derive from the same experiment but different gels for HMGA1, FASN, another for CPT1A and another for β-actin were processed in parallel. β-actin served as loading control (The quantification provided under the blots is for the representative blot from 3 independent experiments). e The correlation between HMGA1 and FASN in CRC patients from the TCGA database. f Representative IHC staining of HMGA1 and FASN in human colorectal and CRC tissues (Scale bar = 20 μm). g Representative images of IHC staining for FASN in the coloretum (CRC) from Rosa26^Hmga1/+ and Hmga1^IEC-OE/+ mice induced with or without AOM/DSS (Scale bar = 20 μm) (n = 12 mice per group). h Representative images of IHC staining for FASN in the colorectum (CRC) from Hmga1^flox/flox and Hmga1^△IEC mice induced with or without AOM/DSS (Scale bar = 20 μm) (n = 12 mice per group). Data are presented as mean ± SD. Statistical significance was determined by two-tailed unpaired t-test (c, d, g, h), two-tailed paired t-test (f), permutation test (b), or Pearson correlation coefficient (e). GSEA: gene set enrichment analysis, TCGA: The Cancer Genome Atlas. Source data are provided as a Source Data file.