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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Mol Cancer Res. 2016 Sep 16;14(12):1182–1194. doi: 10.1158/1541-7786.MCR-16-0111

Figure 1. AMPK activation reduces proliferation through mTOR mediated control of p27.

Figure 1

A-B HTB2 (A.) and HT1376 (B.) bladder cancer cells were treated with 0.5mM AICAR for 72 hours and cell proliferation was assessed by direct cell count. C-D. Cell cycle analysis of HTB2 (C.) and HT1376 (D.) cells treated with 1mM AICAR for 24 hours. E-F. HTB2 (E.) and HT1376 (F.) were treated with 0.5mM AICAR for 24 hours and immunoblot analysis for p-AMPKα, p-ACC, p-S6 and p27 was performed. β-actin was used as a loading control. G-H. HTB2 (G.) and HT1376 (H.) bladder cancer cells were treated with 5nM rapamycin for 24 hours and immunoblot for p-S6, p27 and β-actin was performed. I-J. HTB2 (I.) and HT1376 (J.) were treated simultaneously with Rapamycin (5nM) and compound C (5μM) for 24 hours and immunoblot for p27, p-S6 and β-actin was performed. Statistical significance indicated as; *p<0.05, **p<0.01, ***p<0.001