We demonstrated that deregulation of SP1 in CRC is due to disequilibrium of SP1/miR-320a negative reciprocity, which promotes MACC1 transcription and leads to activation of MACC1-mediated c-MET and downstream signaling pathways, eventually influencing the malignant characteristics of CRC (Fig. 7). This evidence concerns the gene SP1 and colorectal carcinoma.