Fig. 5

SLC27A2 reprogrammed colorectal cancer nongenic crosstalk regulation of PPARs. A The protein expression levels of SLC27A2, PPARG, p-GSK3β, GSK3β, p-Erk, and Erk when SLC27A2 was overexpressed. The grouping of blots cropped from diferent gels. The blots were cut prior to hybridisation with antibodies. The raw data with detail description and multiple exposure images was shown in Supplementary Fig. 1. The relative levels of SLC27A2, PPARG, p-GSK3β/GSK3β, and p-Erk/Erk in HCT-15 and SW480 between NC group and OE group. C The protein expression levels of SLC27A2, PPARG, p-GSK3β, GSK3β, p-Erk, and Erk when SLC27A2 wasknocked down. The grouping of blots cropped from diferent gels. The blots were cut prior to hybridisation with antibodies. The raw data with detail description and multiple exposure images was shown in Supplementary Fig. 1. D The relative levels of SLC27A2, PPARG, p-GSK3β/GSK3β, and p-Erk/Erk in HCT-15 and SW480 between siNC group and siR3 group. E The graphic abstract of SLC27A2 reprogramming colorectal cancer. SLC27A2: Solute carrier family 27 member 2; NC: negative control; OE: over expression; PPARG: Peroxisome proliferator activated receptor G; GSK3β:Glycogen Synthase Kinase 3 Beta; PPARG: Peroxisome proliferator activated receptor G; RXR: retinoid X receptor; FAs: Fatty acids; FATP2: Fatty acid transport protein 2