Fig 1: LPCAT4 increased the expression levels of cholesterol biosynthesis via up-regulating ACSL3. (A) Cholesterol synthesis ability was analyzed in LPCAT4 down-regulation and control group. (B, C) ACSL3 mRNA and protein expression levels were analyzed by RT-PCR and western blot assays, respectively. (D) Overexpression of LPCAT4 increased cholesterol biosynthesis, while knockdown of ACSL3 dismissed this effect. (E) Down-regulation of LPCAT4 decreased cholesterol biosynthesis, while overexpression of ACSL3 could counteract this effect.
Fig 2: Identification of LPCAT4 biological function in LIHC. (A) LPCAT4 mRNA expression level was examined by RT-PCR assay. (B) LPCAT4 protein expression level in LIHC tissues. (C) Western blot assay was used to examine LPCAT4 protein down-regulation efficiency. (D) MTT assay was used to analyze cell growth. (E) Colony formation ability in LPCAT4 down-regulation and control group.
Fig 3: Functional enrichment analysis of LPCAT4 in LIHC. (A) Volcano plot indicated the significantly down-regulated and up-regulated DEGs. (B) GO analysis of DEGs. (C) KEGG analysis of DEGs.
Fig 4: LPCAT4 regulated ACSL3 expression via WNT/ß-catenin/c-JUN signaling pathway. (A) GSEA analysis indicated that WNT signaling pathway was found to be significantly enriched in the high LPCAT4 expression group. (B) Western blot assay was used to examine protein expression level. (C) The three transcription factor-binding sites of c-JUN on potential ACSL3 promoter region were indicated. (D) RT-PCR was used to examine ACSL3 mRNA expression. (E) The ChIP assay was used to validate binding domains of c-JUN in the potential ACSL3 promoter. (F) The luciferase assay was used to confirm which binding sites were functional. (G, H) Western blot assay was used to examine protein expression level.
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