Fig. 8

SRSF5 promoted tumor proliferation in PC cells by promoting cyclinL2^△exon6.3 skipping. a–e PANC-1 cells were infected with control lentivirus, or lentivirus expressing cyclinL2^{△exon6.3- (CCNL2-L)} or cyclinL2^{△exon6.3+ (CCNL2-S)}. The colony formation ability (a, b), cell proliferation ability (c, d), and migration and invasion ability (e) of the indicated stable cells were evaluated. f–h PANC-1 cells were infected with control lentivirus, or lentivirus expressing WT SRSF5, or lentivirus expressing WT SRSF5 and CCNL12-L-specific siRNA. The colony formation ability (f), cell proliferation ability (g), and migration and invasion ability (h) of the indicated stable cells were evaluated. i–k PANC-1 cells were infected with control lentivirus, or lentivirus expressing METTL14-L, or lentivirus expressing METTL14-S and CCNL12-L-specific shRNA. The cell proliferation ability (i, j), and migration and invasion ability (k) of the indicated stable cells were evaluated. l, m PANC-1 cells were infected with control lentivirus, or lentivirus expressing CCNL12-L, or lentivirus expressing CCNL12-L and METTL14-L-specific siRNA. The cell proliferation ability (l), and migration and invasion ability (m) of the indicated stable cells were evaluated. n, o The protein levels of p21, p53 (n), E-cadherin, N-cadherin, and Vimentin (o) in PANC-1 cells as described in (f–h) were determined by western blot assays. 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