Mass Spectrometry and Computer Simulation Predict the Interactions of AGPS and HNRNPK in Glioma

Figure 3

Effects of AGPS and HNRNPK on the in vitro proliferation of glioma cells and tumor-related lipid content. (a) After silencing the expression of AGPS in U251, H4, and TJ905 cells, compared with the control group, the cell proliferation in the shR-AGPS1 group and shR-AGPS2 group was inhibited in vitro. ^ashR-AGPS1 vs. control group, ; ^bshR-AGPS2 vs. control group, ; ^cshR-AGPS2 vs. shR-AGPS1 group, ; ^dshR-AGPS1 vs. rescue-HNRNPK group, ; ^eshR-AGPS2 vs. rescue-HNRNPK group, . (b) The content of tumor-related lipids MAGe, LPAe, LPCe, LPEe, PI, PC, and PS was downregulated, but HNRNPK rescue can reverse the above phenotype. MAGe = monoalkylglycerol ether; LPAe = lysophosphatidic acid ether; LPCe = lysophosphatidylcholine ether; LPEe = lysophosphatidylethanolamine ether; PI = phosphatidyl inositol; PC = phosphatidylcholine; PS = phosphatidylserine. Compared with the control group, ; ^#compared with the shR-AGPS1 group, ; ^Δcompared with the shR-AGPS2 group, .

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