Figure 2 | Oncogene

Figure 2

From: The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid β-oxidation

Figure 2

The protective effect of AICAR on cell survival is mediated by AMPK activation. (a) Percent viability following glucose withdrawal is presented for LN229 cells stably transfected with myrAkt in the presence of glucose (+glc; □), the absence of glucose (−glc; ), or the absence of glucose expressing dnAMPK (−glc+dnAMPK; •). (b) Percent viability following glucose withdrawal of LN229 cells expressing myrAkt in the presence of no drug (−glc; ), 1 mM AICAR (−glc+AICAR; □), or transfected with dnAMPK transgene and treated with 1 mM AICAR (−glc+AICAR+dnAMPK; ♦). Data are presented as mean±s.d. of triplicate samples and are representative of three independent experiments. (c) Western blots of phospho-Ser79 ACC (pS79-ACC), phospho-Thr172 AMPK (pT172-AMPK), and actin. Lysates from LN229 cells expressing myrAkt were prepared after cells were cultured in serum-free medium in the presence or absence of glucose/AICAR for 8 h

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