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. 2019 Jun 14;18(2):1922–1930. doi: 10.3892/ol.2019.10480

Figure 5.

Figure 5.

Overexpression of CCL8 reverses the miR-181-mediated inhibition of proliferation, invasion and migration and induction of apoptosis in glioblastoma cell lines. (A) Proliferation of U87 cells transfected with miR-NC, miR-181 and co-transfected with miR-181 and CCL8. (B) Proliferation of A172 cells transfected with miR-NC, miR-181 and co-transfected with miR-181 and CCL8. (C) Invasion of U87 and A172 cells transfected with miR-NC, miR-181 and co-transfected with miR-181 and CCL8. (D) Migration of U87 and A172 cells transfected with miR-NC, miR-181 and co-transfected with miR-181 and CCL8. (E) Apoptosis rate of U87 cells transfected with miR-NC, miR-181 and co-transfected with miR-181 and CCL8; (F) apoptosis rate of A172 cells transfected with miR-NC, miR-181 and co-transfected with miR-181 and CCL8. (G) Expression of CCL8 in glioblastoma and para-carcinoma tissue detected by RT-qPCR (n=80). (H) Expression of CCL8 in glioblastoma negatively correlated with miR-181 expression, analyzed by Spearman's correlation analysis (n=80). All data are shown as the mean ± standard deviation and based on at least three independent experiments. *P<0.05. miR-181, microRNA-181; CCL8, C-C motif chemokine ligand 8; OD, optical density; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; miR-NC, miR-negative control.