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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression

Fig. 7

YY1 transcriptionally regulates METTL16 expression in CRC cells. A Venn diagram showed the possible transcription factors of METTL16 predicted by PROMO and ChIPBase. B Relative mRNA expression of METTL16 in SW620 cells with CEBPB, YY1, VDR, ETS1, TCF4 or XBP1 knockdown was measured by qRT-PCR. C METTL16 protein expression in SW620 cells with CEBPB knockdown was measured by western blotting. D METTL16 protein expression in SW620 and SW480 cells with YY1 knockdown was measured by western blotting. E METTL16 mRNA expression in SW620 and SW480 cells with YY1 knockdown was measured by qRT-PCR. F The YY1 binding sites in METTL16 promoter. (G) ChIP assay was performed in SW620 and SW480 cells to detect the ability of YY1 binding to the METTL16 promoter. H Schematic representation of the mutated promoter in pGL3-Basic-METTL16-luc reporter to investigate the role of YY1 in METTL16 expression. I SW620 cells were co-transfected with pGL3-METTL16-WT-Luc, pGL3-METTL16-Mut1-Luc, pGL3-METTL16-Mut2-Luc, pRL-TK and si-NC or si-YY1 for 24 h. Results were presented as the ratio between the activity of the reporter plasmid and pRL-TK. J Stability of SOGA1 mRNA was detected in SW620 cells with YY1-konckdown and control cells via qRT-PCR at the indicated time after actinomycin D (5 µg/ml) treatment. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001

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