Ectopic expression of FOXM1c could rescue AMPK mediated cell growth inhibition in cervical cancer cells. (A) XTT cell proliferation assay showed that the growth rates of C33A and SiHa cells with ectopic expression of FOXM1c (OE) were significantly increased as compared with empty vector control (VC). C33A and SiHa cells with ectopic expression of FOXM1c showed a less inhibitory effect on cell growth rate as compared with the vector controls upon treatment of metformin (20 mM). (B) Western blot analysis showed that the level of FOXM1 (including exogenous FOXM1c) could not be reduced in SiHa cells when treated with metformin (25 mM) for 24 hrs. (C) The level of p-AMPKα remained constant when C33A cells were treated with FOXM1 specific inhibitor, thiostrepton (5 μM). (D) Depletion of the endogenous FOXM1 by shRNA knockdown approach could not affect the level of p-AMPKα. Both sh1 and sh2 represent two independent pTER–FOXM1 transfections, while C1 and C2 represent the vector controls.