Fig. 4

IFNγ/STAT1 signaling pathway is involved in MTMR2-induced EMT in GC cells. a Microarray heatmap showed differentially expressed genes in sh-MTMR2 BGC823 and mock cells. The color key for the normalized expression data was shown at the top of the microarray heatmap (green means downregulated genes and red represents upregulated genes. b Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the most differentially expressed genes between the sh-MTMR2 BGC823 and mock cells (fold change ≥1.5). All signaling pathways were sorted according to the Z score. c MTMR2 knockdown enhanced the phosphorylation of JAK1/2, but did not affected the phosphorylation of TYK2. d MTMR2 knockdown enhanced the phosphorylation of STAT1, but did not affected the phosphorylation of STAT2 and STAT3. e MTMR2 knockdown not only upregulated the level of pSTAT1, but also enhanced the nuclear accumulation of pSTAT1. f IFNγ treatment (50 ng/mL, 48 h) decreased invasion capability of MGC803 and BGC823 cells, which was attenuated by MTMR2-overexpression. g IFNγ treatment (50 ng/mL, 48 h) enhanced the levels of pJAK1/2 and pSTAT1, accompanying with upregulated E-cadherin and downregulated N-cadherin and vimentin. And these effects of IFNγ treatment were reversed by MTMR2 overexpression. h, i Both JAK inhibitor (15 ng/mL, 48 h) (h) and STAT1 siRNA (40 nmol/L, 48 h) (i) enhanced the invasive capability in control MGC803 and BGC823 cells and reversed the invasive capability reduced by MTMR2 knockdown in sh-MTMR2 MGC803 and BGC823 cells