Fig. 5: CELSR2 KD compromises WNT3A-induced proliferation of U87 MG cells.
From: Atypical cadherin CELSR2 acts as a therapeutic target for glioma through WNT3A/β-catenin signaling
A, B Administration of WNT3A, WNT5A and WNT1 significantly enhanced cell proliferation of cultured glioma cells, as revealed by EDU staining. C, D In CELSR2-KD U87 MG cells, WNT5A and WNT1, but not WNT3A, significantly enhanced cell proliferation as identified by EDU labeling. E, F Flow cytometry showed a decrease in the G0/G1 ratio and an increase in the S phase in the control+WNT3A group (U87 MG cells treated with WNT3A) compared to the control group (U87 MG cells), and no significant change in the KD group (CELSR2-KD U87 MG cells) compared to the KD + WNT3A group (CELSR2-KD U87 MG cells treated with WNT3A). G, H Western blots showed a significant increase of β-catenin and cyclin D1, and a significant decrease in GSK-3β in the Ctrl+WNT3A group compared to the control group, and there was no significant protein change in the KD group compared to the KD + WNT3A group. Scale bar is 50 μm in (A, C). Data are represented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; n = 3, Student’s t-test.
