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 4. NAP1L1 interacts with HDGF and HDGF knockdown reverses the effect of overexpressed NAP1L1 on proliferation of glioma cells. (A) Co-IP experiments detected the interaction of endogenous NAP1L1 and HDGF in U87 and LN229 cells. (B) Representative immunofluorescence staining and intensity of NAP1L1 and HDGF protein in U87 and LN229 cells. Scale bar, 5 μm. (C) HDGF level in U87 and LN229 cells transfected with siNAP1L1 or NAP1L1-overexpressing plasmid. MTT assay (D) and EdU incorporation assay (E) in glioma cells transfected with control or HDGF siRNA. (F) Western blotting analysis of the protein levels of HDGF, NAP1L1 and c-Jun after transfection of siHDGF into glioma cells. GAPDH served as the internal control. Data are presented as the mean ± SD for three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001.