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. 2014 Jan 13;111(4):E435–E444. doi: 10.1073/pnas.1311121111

Fig. 5.

Fig. 5.

Metformin and AICAR inhibit glioma growth in vivo and AICAR inhibits glioma proliferation by degrading cdc25c independent of AMPK. (A) Metformin and AICAR’s effect on growth of control (NT shRNA) and AMPKβ1 shRNA expressing U87EGFRVIII glioma xenografts in Nu/Nu mice (n = 10 per condition). *P ≤ 0.03 shown for both metformin and AICAR in NT and shRNA tumors. (B) Photomicrographs of representative control and treated gliomas. Histogram of the cell cycle analysis of three glioma cells (C) and control (nt) and AMPKβ1-silenced T98G glioma cells (D), treated with AMPK agonists. *P ≤ 0.005. Immunoblots show the effects of AICAR on G2M regulators in two glioma cells (E), and in control (nt) and AMPKβ1shRNA T98G glioma cells (F). (G) Effect of AICAR on cdc25c RNA levels. (H) Effects of AICAR alone or in the presence of the proteasomal inhibitor MG132 on protein levels of cdc25c in control (nt) and β1 shRNA T98G glioma cells. (I) Proliferation and cell cycle analysis of control (nt) and cdc25c shRNA expressing T98G glioma cells. (I, Inset) Immunoblot shows knockdown of cdc25c protein by three independent shRNA. Data are representative of at least three independent experiments. nt, nontarget. *P ≤ 0.005. Error bars in A and I represent mean ± SD.