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 5. HDGF interacts with c-Jun and c-Jun overexpression reverses the effect of HDGF knockdown on proliferation of glioma cells. (A) Co-IP experiments detected the interaction of endogenous HDGF and c-Jun in U87 and LN229 cells. (B) Representative immunofluorescence staining and intensity of HDGF and c-Jun protein in U87 and LN229 cells. Scale bar, 5 μm. (C) c-Jun expression in U87 and LN229 cells transfected with siHDGF or HDGF-overexpressing plasmid. The MTT assay (D) and EdU incorporation assay (E) in glioma cells after transfecting c-Jun-overexpressing plasmid. (F) Western blotting for c-Jun, CCND1, CDK4 and CDK6 in glioma cells after transfected with c-Jun-overexpressing plasmid. 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.