Fig. 2

In vitro inhibitory effect of Lf-GL on GBM progression. a Relative viability of U87MG cells treated with GL equivalent concentrations of 25 μM to 200 μM, respectively, in GL-, Lf-, and Lf-GL- treated groups. Data are expressed as mean ± S.E.M (n = 6). ***P < 0.001 versus GL-treated group. b Monitoring tumor progression for 3 days in GL-, Lf-, and Lf-GL- treated U87MG cell. Data are expressed as mean ± S.E.M (n = 6). ***P < 0.001 versus GL-treated group. c Investigation of HMGB1-mediated GBM cell proliferation and its inhibitory ability of GL and Lf-GL for 3 days. Data are expressed as mean ± S.E.M (n = 8). d Wound healing assay to investigate HMGB1-mediated GBM cell migration and its inhibitory effect of GL, Lf, and Lf-GL. Data are expressed as mean ± S.E.M (n = 3). Red dashed lines indicate starting point. Blue dashed lines mark the location where the U87MG cells migrated over 24 h. Scale bar: 500 μm. e Inhibitory effect on tumor migration distance of Con-, GL-, Lf- and Lf-GL treatment groups according to the presence or absence of HMGB1. HMGB1 (-) indicates absence of HMGB1 treatment. HMGB1 ( +) indicates the presence of HMGB1 treatment. Data are expressed as mean ± S.E.M (n = 3). **P < 0.01 and ***P < 0.001. f Mechanism of cellular uptake of Lf-GL-FITC for 18 h by co-staining with DAPI and Lysotracker. g HMGB1 concentration in the medium of U87MG cells in different treatment groups. Data are expressed as mean ± S.E.M (n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001Data are expressed as mean ± S.E.M (n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001