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. 2018 Dec 5;11:8491–8505. doi: 10.2147/OTT.S178455

Figure 4.

Figure 4

FAM3C reduction inhibited EMT and suppressed PI3K–Akt pathway activation in gastric cancer cells.

Notes: (A) Immunofluorescence of E-cadherin, vimentin, and FAM3C. E-cadherin was upregulated in FAM3C-knockdown MKN45 cells. The expression of vimentin in FAM3C-knockdown cells was decreased, as was mesenchymal cell morphology. Bar 50 µm. (B) Pattern diagram of the KEGG pathway enrichment of genes positively related to FAM3C in the gastric adenocarcinoma database of TCGA. Pathways with P<0.05 and >5% associated genes are shown. Each circle represents a KEGG pathway term or a gene. (C) Western blotting showed that knockdown of FAM3C caused increased expression of E-cadherin and decreased levels of p-Akt, p-GSK3β, Snail, and Slug (due to the mutation of E-cadherin in AGS cells, we could not detect E-cadherin by Western blotting in AGS cells).

Abbreviations: ECM, extracellular matrix; EMT, epithelial–mesenchymal transition; KEGG, Kyoto Encyclopedia of Genes and Genomes; NC, negative control; TCGA, the Cancer Genome Atlas.