Skip to main content
Fig. 6 | Cell & Bioscience

Fig. 6

From: N6-methyladenosine-mediated CELF2 regulates CD44 alternative splicing affecting tumorigenesis via ERAD pathway in pancreatic cancer

Fig. 6

CELF2 made CD44 form different spliceosomes to exert anti-tumor effects. A An alternative splicing model with the alternative splicing genes involved in pancreatic cancer based on the TCGA database was established. B CELF2-mediated CD44 performed alternative splicing. C and D Protein levels of the different spliceosomes of CD44 after CELF2 overexpression were analyzed by western blot. E and F The different CD44 spliceosomes were detected after CELF2 overexpression in BxPC-3 and MIA PaCa2 cells by RT-PCR. Compared with the control group, the expression of CD44s was significantly decreased after overexpression of CELF2, while the expression levels of nine other spliceosomes, but not CD44v6, were increased. The results are consistent with the observed changes in CD44 mRNA spliceosome levels. Abbreviations in Additional file 1: Figure S1A: AA alternate acceptor, AD alternate donor site, AP alternate promoter, AT alternate terminator, ES exon skip, ME mutually exclusive exons, RI retained intron. The data are expressed as mean ± SD of three replicates. *P < 0.05, **P < 0.01

Back to article page