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Fig. 8 | Journal of Hematology & Oncology

Fig. 8

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

Fig. 8

SRSF5 promoted tumor proliferation in PC cells by promoting cyclinL2exon6.3 skipping. ae PANC-1 cells were infected with control lentivirus, or lentivirus expressing cyclinL2exon6.3- (CCNL2-L) or cyclinL2exon6.3+ (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. fh 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. ik 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 (fh) 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

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