In this study, we revealed that (1) high MIR17HG expression predicted poor prognosis in CRC patients, especially in patients with liver metastasis; (2) MIR17HG functioned as a ceRNA to regulate HK1 expression by sponging miR-138-5p, which promoted aerobic glycolysis and liver metastasis in CRC; and (3) glycolysis-accelerated lactate accumulation promoted MIR17HG transcription via the p38/Elk-1 pathway, thus forming a positive feedback loop. Here, HK1 is linked to colorectal carcinoma.