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. 2022 Nov 7;8:449. doi: 10.1038/s41420-022-01234-8

Fig. 3. LINC01468 activates Akt/mTOR signaling pathway.

Fig. 3

A Differently expressed genes in SNU-449 cells transfected with shLINC01468 or control were shown by heatmap. B KEGG pathway analysis of LINC01468-regulated genes. C KEGG pathway enrichment analysis of target genes by a bubble chart. The size and color of the dots represents the number and level of genes that were enriched in the corresponding pathways, respectively. D The item was enriched using GSEA in SUN-449 cells transfected with shLINC01468 or control. E, F Immunoblot detection of Akt/mTOR signaling pathway protein level in E LINC01468-knockdown SNU-449 cells or F LINC01468-overexpressed Huh7 cells. G Immunoblotting of the indicated protein lysates from Huh7 cells expressing Ctrl or LINC01468 treated with or without rapamycin (Rapa). H The intracellular lipid droplets in SUN-449 cells transfected with shLINC01468 or control were stained with oil red O. I The cellular content of triglycerides and phospholipids in the indicated cells in H was detected. J Representative liver images (top), H&E staining (middle), and ORO staining (bottom) of xenografts derived from SUN-449 cells stably transfected with the scrambled control or siLINC01468. KM Overexpression of LINC01468 increased tumor growth and mediated sorafenib resistance of HCC tumors in nude mice. Images show representative tumor (K). Growth curves (L) and tumor weights (M) of mean ± SD of six mice in each group.***P < 0.005; ****P < 0.001.