Fig. 5: DUSP5P1 exerts tumor-promoting function partially depending on the ARHGAP5.

A, B ARHGAP5 mRNA A and protein expression B were correlated with the DUSP5P1 expression. Ectopic expression of DUSP5P1 increased the mRNA and protein expression of ARHGAP5 in BGC823, MGC803 and GES1 by qRT-PCR and Western blot. C DUSP5P1 expression positively correlated with ARHGAP5. D Representative images of ARHGAP5 protein expression in primary GC tissues by IHC (left panel). ARHGAP5 expression significantly higher in the GC tissue as compared with adjacent non-cancer tissues (right panel). E Successful knockdown of ARHGAP5 in AGS and MKN74 cells was confirmed by RT-PCR and Western blot. F ARHGAP5 knockdown inhibited cell migration and invasion. G Pro-metastatic function of DUSP5P1 is dependent on ARHGAP5. (G1) Knockdown of ARHGAP5 significantly blunted the promoting effects of DUSP5P1 on cell migration and invasion. (G2) Effect of DUSP5P1 knockdown on migration ability with or without ARHGAP5 overexpression was investigated. ARHGAP5 overexpression significantly blunted the inhibiting effects of DUSP5P1 knockdown on cell migration. H ARHGAP5 activated MAPK signaling. H1: ARHGAP5 activated MAPK signaling as evidenced by SRE luciferase reporter assay (left panel); H2: The effectors of MAPK signaling pathway regulated by ARHGAP5 identified by MAPK signaling pathway PCR array; H3: Correlation analysis of ARHGAP5 and effector genes form TCGA database. I Effect of DUSP5P1 on MAPK pathway with or without ARHGAP5 knockdown was detected by SRE luciferase reporter assay. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.001.