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Fig. 9 | Journal of Hematology & Oncology

Fig. 9

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

Fig. 9

Aberrant alternative splicing of METTL14exon10 and CyclinL2exon6.3 possessed prognostic values for PDAC patients. a PCR of cyclinL2exon6.3 and METTL14exon10 in PDAC samples was evaluated by PCR. Representative images of DNA gel electrophoresis are shown. bd The correlations between the levels of METTL14exon10 (b) or CyclinL2exon6.3 (c) and the expression levels of p-SRSF5 and their correlations (d) were determined by IHC staining in tumor tissues were performed. e, f The correlations between the levels of METTL14exon10 (e) or CyclinL2exon6.3 (f) and lymphatic metastasis and tumor size. g, h Multiple-factor analysis between CLK1-SRSF5-METTL14/SRSF5 axis and lymphatic metastasis and tumor size. Il Overall and disease-free survival analyses were performed to assess the impact of PSI of METTL14exon10 or CyclinL2exon6.3 shift in PDAC patients. m A proposed working model of the CLK1-SRSF5 axis induced aberrant exon skipping of m6A methyltransferase METTL14 and Cyclin L2 in promoting the development of the pancreatic cancer through regulating cell cycle progression, cell proliferation, and metastasis. Overall (a, c) and disease-free (b, d) survival analyses were performed to assess the impact of PSI of METTL14exon10 or CyclinL2exon6.3 shift in PDAC patients in external corhort

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