Additional file 6 of CLK1/SRSF5 pathway induces aberrant exon skipping of METTL14 and Cyclin L2 and promotes growth and metastasis of pancreatic cancer

Additional file 6: Figure S5. CLK1-mediated SRSF5 phosphorylation on Ser250 contributed to the malignant behaviors of pancreatic cancer cells. (A-E) BxPC-3 cells were infected with control lentivirus, or lentivirus expressing wild type (WT)/mutated (S250MU)/phosphorylated (S250P) SRSF5. The cell proliferation ability (A, B), colony formation ability (C), and migration and invasion ability (D, E) of the indicated stable cells were evaluated. (F-J) PANC-1 cells were infected with control lentivirus or lentivirus overexpressing CLK1 or lentivirus overexpressing CLK1 together with shSRSF5. The cell proliferation ability (F, G), colony formation ability (H), and migration and invasion ability (I, J).The stable cells were infected with control lentivirus, or lentivirus expressing wild type (WT)/mutated (S250MU)/phosphorylated (S250P) SRSF5 were simultaneous treatment with TG003 (K–O)were evaluated. The cell proliferation ability (K, L), colony formation ability (M), and migration and invasion ability (N, O). (P)The quantification of the results of Fig. 5B. (Q, R)The quantification of the results of Fig. 5K. n = 3 for each group; data are shown as mean ± SD from three independent experiments.*P