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Fig. 7 | Journal of Hematology & Oncology

Fig. 7

From: CLK1/SRSF5 pathway induces aberrant exon skipping of METTL14 and Cyclin L2 and promotes growth and metastasis of pancreatic cancer

Fig. 7

SRSF5 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 groups

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