Confirming the positive impact of the LINC00183-ENO1 interaction on the glycolytic capacity of CRC cells, ENO1 overexpression reversed the suppression of lactate production, ATP generation, and glucose consumption mediated by LINC00183 silencing, whereas sh-ENO1 transfection significantly reversed the pro-glycolytic effects induced by LINC00183 overexpression (Fig. 7C and Supplementary Fig. S3D–G, and H–O). This evidence concerns the gene ENO1 and colorectal carcinoma.