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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: MAGOH promotes gastric cancer progression via hnRNPA1 expression inhibition-mediated RONΔ160/PI3K/AKT signaling pathway activation

Fig. 8

MAGOH accelerated GC progression by activating the PI3K/AKT signaling pathway in an hnRNPA1/RONΔ160-dependent manner. A The enrichment of DEGs in different pathways was assessed by KEGG pathway enrichment analysis. B WB was used to detect changes in the expression of PI3K/AKT signaling pathway components and their corresponding downstream genes in GC cells after MAGOH knockdown, MAGOH overexpression or stable MAGOH knockdown followed by MAGOH restoration. C WB was used to assess the expression of proteins in the PI3K/AKT signaling pathway in the MAGOH-silenced and hnRNPA1-silenced rescue groups of GC cells. D WB was used to assess the expression of proteins in the PI3K/AKT signaling pathway in the MAGOH-silenced and RONΔ160-overexpressing rescue groups of GC cells. EG A CCK8 assay was performed to evaluate the proliferative ability of MAGOH-overexpressing (E), hnRNPA1-silenced (F) and RONΔ160-overexpressing (G) GC cells in the presence of LY294002, an inhibitor of the PI3K/AKT signaling pathway

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