Fig. 2From: CLK1/SRSF5 pathway induces aberrant exon skipping of METTL14 and Cyclin L2 and promotes growth and metastasis of pancreatic cancerCLK1 enhanced the proliferation ability of human pancreatic cancer cells in vitro and in vivo. a, b BxPC3 cells with stable CLK1 overexpression (a) and PANC-1 cells with CLK1 knockdown (b) were generated. The changes in CLK1 expression were confirmed using western blot assays. c–i The proliferative ability of stably transfected PANC-1 or BxPC3 cells was investigated via colony formation assays (c–e) and CCK-8 assays (f–i). Representative colony formation images are shown (c, d), and the numbers of colonies were summarized (e). j, k Flow cytometry analysis of the cell cycle progression of stably transfected PANC-1 (k) or BxPC3 (j) cells was performed. Representative images and quantification of the results are presented. l–n Overexpression of CLK1 promoted the growth of BxPC-3 cells in a subcutaneous xenograft mouse model (l–n). The size of the tumors was measured at the indicated time points (m, ***P < 0.001). Tumors were extracted and weighed after mice were sacrificed (n, ***P < 0.001). CLK1 knockdown inhibited the growth of PANC-1 cells in a subcutaneous xenograft mouse model (l, o, p). The size of the tumors was measured at the indicated time points (o, ***P < 0.001). Tumors were extracted and weighed after mice were sacrificed (p, ***P < 0.001). q The protein levels of p21 and p53 were quantitated by western blot assays, and representative images are shown. 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