Fig. 6

SNHG17 binding to PGK1 enhanced phosphorylation of the T168A site of PGK1 in THP-1 cell-derived TAMs. A and D THP-1 cells (shNC, sh1-SNHG17, sh2-SNHG17, NC, and SNHG17-OE) stably expressing Flag-PGK1 were co-cultured with PCs (PANC-1 or PATU-8988 cells) for 48 h. PD, pull-down. B Flag-PGK1 protein was pulled down from THP-1 cell-derived TAMs stably expressing Flag-PGK1 WT or PGK1 T281A, T168A, or T378A. C THP-1 cell-derived TAMs stably expressing Flag-PGK1 WT, PGK1 T168A, or PGK1 T168D were harvested. PGK1 pT168, phospho-PGK1 T168. E The binding ability of SNHG17 to PGK1 or mutated-PGK1 at the T168A site was analyzed by RNA pull-down assay. F-I Flow cytometric analysis of the expression of M1 markers (CD80 and CD86) and M2 markers (CD163 and CD206) in THP-1 cell-derived TAMs transfected with PGK1 overexpression plasmids or PGK1 mutated plasmids. J qPCR analysis of the expression of M2 markers and M1 markers in THP-1 cells co-cultured with PANC-1 cells (NC, PGK1-WT, PGK1-MUT). K-L CCK8 analysis of PANC-1 cells (K) or PATU-8988 cells (L) co-cultured with THP-1 cells transfected with PGK1 overexpression plasmids or mutated PGK1 plasmids. M–O Transwell assays were used to assess the migratory or invasive abilities of PANC-1 or PATU-8988 cells co-cultured with THP-1 cells. P-S Lactic acid concentration (P-Q) and glucose uptake (R-S) analysis of THP-1 cell-derived TAMs in each group (NC, PGK1-WT, and PGK1-MUT)