Fig. 7From: CLK1/SRSF5 pathway induces aberrant exon skipping of METTL14 and Cyclin L2 and promotes growth and metastasis of pancreatic cancerSRSF5 elevated the m6A level and promoted cell proliferation and metastasis in PC cells by inhibiting METTL14 exon10+ skipping. a, b m6A immunoprecipitation assays were performed to determine the m6A levels in PANC-1 cells transduced with control vector plasmid, or plasmids expressing wild type (WT)/ phosphorylated (S250P) SRSF5 (a) or PANC-1 cells infected with control lentivirus, or lentivirus expressing METTL14-L or METTL14-S (b). c–h The proliferation ability (c, f), colony formation ability (d, e), migration and invasion ability (g, h) of PANC-1 cells infected with control lentivirus, or lentivirus expressing METTL14-L or METTL14-S were evaluated. i–l The m6A levels (i), colony formation ability (j), cell proliferation ability (k), migration and invasion ability (l) of PANC-1 cells infected with control lentivirus, or lentivirus expressing WT SRSF5 or WT SRSF5 together with METLL14 exon10-specific shRNA were evaluated. m–o The m6A levels (m), colony formation ability (n), cell proliferation ability (o) of PANC-1 cells infected with control lentivirus, lentivirus expressing SRSF5-specific siRNA alone, or SRSF5-specific siRNA together with METTL14-L or METTL14-S were evaluated. Representative images and quantification of the results are presented. n = 3 for each group; data are shown as mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001, between the indicated groupsBack to article page