Research Paper Volume 13, Issue 24 pp 26180—26200

NAP1L1 promotes proliferation and chemoresistance in glioma by inducing CCND1/CDK4/CDK6 expression through its interaction with HDGF and activation of c-Jun


Figure 3. NAP1L1 controls the expression of cell cycle and apoptosis associated genes via the CCND1/CDK4/CDK6 signaling pathways in glioma. EdU incorporation assay (A), Cell cycle analysis (B), Cell apoptosis assay (C) Mitochondrial membrane potential assay (D) in U87 and LN229 cells transfected with control siRNA (siNC) or NAP1L1 siRNA (siNAP). (E) Western blotting analysis of the protein levels of CCND1, CDK4, CDK6, Bcl-2 and cleaved caspase3 after transfecting siNC or siNAP into U87 and LN229 cells. (F) The H&E of the nude mice tumor tissues. NAP1L1, Ki67, and PCNA was evaluated by immunohistochemical staining. Compared with shNAP cells, the shNC cell tumor tissues were high expression. *P < 0.05, **P < 0.01, ***P < 0.001.