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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: SNHG17 alters anaerobic glycolysis by resetting phosphorylation modification of PGK1 to foster pro-tumor macrophage formation in pancreatic ductal adenocarcinoma

Fig. 7

SNHG17 formation of SNHG17/PGK1/ERK1/2 complex promoted phosphorylation at the T168A site of PGK1. A The level of phosphorylation of PGK1 in THP-1 cell-derived TAMs (sh-ERK1/2 and ERK1/2-OE). B-C RNA pull-down and WB analysis of SNHG17 interacting with the ERK1/2 and PGK1 proteins in THP-1 cells transfected with shRNA of SNHG17 (B) and PGK1 (C). D-E The protein expression level of ERK1/2 in THP-1 cell-derived TAMs (sh-PGK1 and PGK1-OE (D) and sh-SNHG17 and SNHG17-OE (E)). F ERK1/2 expression levels in macrophages isolated from subcutaneous tumors (n = 4) (G-H) RIP-qPCR was utilized to identify the interaction between SNHG17 and PGK1 in THP-1 cells (ERK1/2 overexpression (G) and ERK1/2 knockdown (H)) co-cultured with PANC-1 or PATU-8988 cells. I Immunoblot analysis of the ability of PGK1 to bind directly to SNHG17 in THP-1 cell-derived TAMs after knockdown of ERK1/2. J Graphical summary of the major findings in this study

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