Fig. 4: PKM2 acted as a key regulator in TGF-βRII mediating glycolysis in oral CAFs. | Cell Death Discovery

Fig. 4: PKM2 acted as a key regulator in TGF-βRII mediating glycolysis in oral CAFs.

From: TGF-βRII regulates glucose metabolism in oral cancer-associated fibroblasts via promoting PKM2 nuclear translocation

Fig. 4

A Cytoscape visualization of the protein network in glycolysis with combined analysis of TGF-β and HIF-1α signaling pathways. Protein–protein interaction network and transcriptional factor co-mediating glycolysis and TGF-β signaling pathway were generated by String and visualized by Cytoscape. PKM2 exhibited a closer relationship with the TGF-β signaling pathway than HIF-1α in this network analysis. B, C By 2-dimensional electrophoresis (2-DE) staining in proteomics analysis of glycose metabolism, PKM2 was downregulated by the overexpressed TGF-βRII in CAFs (fold change of PKM2 was 2.13021). D, E By western blot (WB), c-Myc, and SP1 were decreased by upregulation of TGF-βRII while SP3 was increased in CAFsTGF-βRII when compared to CAFsEV and CAFs, respectively. F, G Immunoblot showed a reduction of phosphorylated Smad2/3 in CAFsTGF-βRII while no obvious change of total Smad2/3. H–J Immunoblot showed a reduction of phosphorylated P38 and mTOR, however, no obvious difference of total P38, JNK, mTOR, and p-JNK among the groups was observed. The relative protein expression level was quantified after normalization to GAPDH. n = 3 independent experiments; error bars, mean ± SD; n.s. not significant, *P < 0.05, ***P < 0.001; t test.

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