Fig. 3

LncSLCC1 drives glycolytic metabolism to activate CRC proliferation. a ssGSEA analysis was performed to show the pathways closely correlated with lncSLCC1 expression in control and lncSLCC1 downregulated cells. b–d Lactate concentration (b), ATP production (c), and ECAR (d) were detected in control and lncSLCC1-knockdown DLD-1 cells. e–g Lactate concentration (e), ATP production (f), and ECAR (g) were measured in control and lncSLCC1-overexpression HT29 cells. h Representative images of 18F-FDG uptake by micro-PET imaging in control and lncSLCC1-knockdown xenograft mouse models. White circles indicated tumor glucose uptake. Maximum uptake values (SUVmax) for xenografts measured by FDG PET were presented. i, j Cell proliferation (i) and colony formation (j) were measured in DLD-1 cells after transfected with Control or lncSLCC1-smart silencer. k–m Representative images of tumors (k), tumor weights (l), and tumor volumes (m) were measured in nude mice bearing DLD-1 cells transfected with control shRNA or lncSLCC1 shRNA, n = 5. n, o Cell proliferation (n) and colony formation (o) were measured in HT29 cells after transfection with control or lncSLCC1-overexpression plasmid. p, q Cell proliferation (p) and colony formation (q) were measured in HT29 cells transfected with pCDNA3.1 and pCDNA3.1-lncSLCC1 plasmid treated with or without glycolysis inhibitor 2-DG