Figure 6.

Accumulated palmitic acid is responsible for activation of β-catenin signaling. (A) Lipidomics was applied and the expression level of palmitic acid (PA) was analyzed in CRC tumors or shNudt7 introduced Kras^WT CRC cells (left panel) (n = 4). The efficiency of shNudt7 was confirmed using Kras^WT CRC cells (right panel). (B) Kras^WT Caco2 cells were introduced with Nudt7 or shNudt7 in the presence of PA and the expression level of β-catenin was analyzed by real-time PCR and represented as the fold change compared with the negative control (-palmitic acid/-shNudt7/-Nudt7). Results are representative of at least 3 independent experiments. Rn18s was used as an endogenous control. (C) Schematic diagram of generating Chi or Chi/PA film. (D) Chi or Chi/PA film was attached in the colon of Nudt7^+/+ mice for one week and polyp number was counted. Scale bars: 0.5 cm. (E) Immunohistochemistry with H&E, NUDT7, Ki67, CD45, β-catenin, PCNA, and F4/80 (n = 5) colon-attached Chi or Chi/PA film. Results are representative of at least 3 independent experiments and for every 100 cells in 3 different fields at 100× magnification. Scale bars: 200 μm. (F) Expression level of CRC-related genes in colon-attached Chi or Chi/PA film and represented as the fold change compared with colon-attached Chi film. Results are representative of at least 3 independent experiments. * p ≤ 0.05, ** p < 0.01, *** p < 0.01, **** p < 0.0001.