Fig. 7: NFE2L3 activates the PI3K/AKT pathway by regulating LASP1. | Cell Death & Disease

Fig. 7: NFE2L3 activates the PI3K/AKT pathway by regulating LASP1.

From: NAT10 promotes the progression of clear cell renal cell carcinoma by regulating ac4C acetylation of NFE2L3 and activating AKT/GSK3β signaling pathway

Fig. 7

a Compared with the control group, RNA-seq results showed that 312 transcripts in the NFE2L3 knockdown group were downregulated and 3 114 transcripts in the ccRCC tissue were upregulated, and ChIP-seq showed that NFE2L3 could bind to the promoter region of 1 618 transcripts. There were 12 overlapping transcripts. b The expression levels of 12 overlapping transcripts in control cells and knockdown NFE2L3 cells were analyzed by heat map. c The mRNA of NFE2L3 and LASP1 decreased after NAT10 knockdown in 786-O cells by QRT-PCR. d QRT-PCR detected the decrease of LASP1 mRNA after NFE2L3 knockdown in 786-O cells. e NFE2L3 was detected by ChIP-qPCR to bind to the promoter of LASP1. f The binding sites of NFE2L3 and LASP1 transcripts mainly occur in the common sequences. g Dual luciferase assay showed that NFE2L3 could regulate the LASP1 promoter region. h After NFE2L3 knockdown, LASP1 and β-catenin expression was decreased, AKT/GSK3β phosphorylation was inhibited. i After NAT10 knockdown, the expressions of NFE2L3, LASP1 and β-catenin were decreased, the phosphorylation of AKT/GSK3β was inhibited. j The expression of LASP1 and phosphorylation of AKT/GSK3β were not changed after NAT10 knockdown in the NFE2L3 knockdown cells, nor was the expression of β-catenin. k The TCGA database showed that LASP1 was highly expressed in ccRCC. l The correlation of NFE2L3 and LASP1 mRNA in 20 ccRCC tissues was performed, r = 0.71181, p < 0.0005.

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