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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Long non-coding RNA NEAT1 mediated RPRD1B stability facilitates fatty acid metabolism and lymph node metastasis via c-Jun/c-Fos/SREBP1 axis in gastric cancer

Fig. 3

RPRD1B facilitates fatty acid uptake and synthesis by activating the c-Jun/c-Fos/SREBP1 axis. A The KEGG pathways and functional annotations were analyzed from a transcriptome analysis identifying genes that are upregulated upon RPRD1B overexpression. Enriched terms involved in RPRD1B function were the MAPK pathway, Wnt pathway, and fatty acid metabolism. B Representative GSEA plots were enriched in AP1 and SREBP1 transcriptional activity upon RPRD1B overexpression. C Relative mRNA levels of fatty acid metabolism-related genes were examined in LacZ- and RPRD1B-, Scr- and shRPRD1B-stably transfected cells as determined using qRT–PCR. D A schematic diagram of pathways identified in the KEGG pathway analysis and functional annotations. RPRD1B activated fatty acid metabolism through the c-Jun/c-Fos/SREBP1 pathway. E, F Cellular cholesterol and triglyceride levels were assessed in GC cells with RPRD1B knockdown or overexpression. G Oil Red O staining showing lipid droplets in GC cells with RPRD1B knockdown or overexpression. Scale bar, 50 μm. H Levels of the RPRD1B, c-Jun, c-Fos, SREBP1, FASN, ACSS2 and FABP3 proteins were determined in LacZ- and RPRD1B-, Scr- and shRPRD1B-stably transfected cells. GAPDH served as a loading control. Data are presented as the means ± SD of three independent experiments. (**, P < 0.01; ***, P < 0.001)

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