Skip to main content
Fig. 4 | Molecular Cancer

Fig. 4

From: p113 isoform encoded by CUX1 circular RNA drives tumor progression via facilitating ZRF1/BRD4 transactivation

Fig. 4

p113/ZRF1/BRD4 complex promotes lipid metabolic reprogramming and mitochondrial complex I activity in NB cells. a Heatmap, distribution, and binding motif of ChIP-Seq (left panel) assay revealing genomic enrichment of ZRF1 in SH-SY5Y cells, while Venn diagram, heatmap, and GO pathway (right panel) showing identification of p113/ZRF1/BRD4 target genes by overlapping analysis of RNA-seq results upon p113 over-expression and ChIP-seq peaks of ZRF1 or BRD4. b ChIP-seq assay showing the binding peak of BRD4 or ZRF1 on promoter regions of ALDH3A1, NDUFA1, or NDUFAF5 in SH-SY5Y cells. c Western blot assay indicating the expression of ALDH3A1, NDUFA1, or NDUFAF5 in SH-SY5Y cells stably transfected with empty vector (mock) or ecircCUX1, and those co-transfected with sgRNA specific against ZRF1 or BRD4 for CRISPRi. d Schematic illustration showing the involvement of ALDH3A1, NDUFA1, or NDUFAF5 in lipid metabolic reprogramming and mitochondrial respiratory activity. e Relative OCR levels in SH-SY5Y cells stably transfected with mock or ecircCUX1, and those co-transfected with sgRNA specific against ZRF1 or BRD4 for CRISPRi (n = 5). f Relative fatty acid levels, complex I activity, NAD+/NADH ratio, and ATP levels in SH-SY5Y cells stably transfected with mock or ecircCUX1, and those co-transfected with sgRNA specific against ZRF1 or BRD4 for CRISPRi (n = 5). ANOVA compared the difference in e and f. *P < 0.05 vs. mock+CRISPRi-Scb. Data are shown as mean ± s.e.m. (error bars) and representative of three independent experiments in c, e and f

Back to article page