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Fig. 3 | Molecular Cancer

Fig. 3

From: WTAP facilitates progression of hepatocellular carcinoma via m6A-HuR-dependent epigenetic silencing of ETS1

Fig. 3

A high-throughput sequencing combination revealed ETS1 to be the target of WTAP. a Transcriptome profiles from Huh7 cells transfected with the WTAP siRNAs or negative control siRNAs (both in triplicate) were shown. Bands with red, black or green in the heat map indicated high, moderate or low expression, respectively. b A Venn diagram was generated from the gene sets enriched for transcripts that were substantially altered after WTAP silencing (RNA-seq), along with those enriched for m6A-modified transcripts (m6A-seq) and those enriched for WTAP-conjugated transcripts (CLIP-seq). 15 genes were selected according to the overlaps. The RNA-seq data was acquired from our study, while the m6A-seq and CLIP-seq data were obtained from GEO datasets (GSE46705). Information regarding detailed gene sets of RNA-seq was listed in Additional file 4: Table S4; c, d and e RT-qPCR was performed in Huh7 (c) and PLC/PRF/5 (d) with WTAP silencing, and in HCCLM3 (e) with WTAP overexpression, to validate the overlapped genes. The variation of ETS1 and ETS2 was consistent among 15 genes in the above three cell lines; f and g Expression of ETS1 and ETS2 following WTAP knockdown was evaluated by western blotting and RT-qPCR in Huh7 (f) and PLC/PRF/5 cells (g); h and i Expression of ETS1 was further examined by western blotting and RT-qPCR in Hep3B (h) or HCCLM3 (i) cells following the knockdown or overexpression of WTAP

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