Figure 6 | Oncogene

Figure 6

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

Figure 6

Activation of fatty acid oxidation is both necessary and sufficient to protect Akt-expressing cells from death induced by glucose deprivation. (a) Percent viability was measured daily by propidium iodide exclusion for LN229 cells expressing myrAkt. Cells were plated at 2 × 105 cells/well and maintained in serum-free medium for 24 h before shifting to medium lacking glucose with no drug (−glc; ), with 1 mM AICAR (−glc+AICAR; □), or with 1 mM AICAR and 60 μ M etomoxir (−glc+AICAR+ETO; •); or (b) cells were incubated in medium containing glucose in the presence of no drug (+glc; ), or 1 mM AICAR and 60 μ M etomoxir (+glc+AICAR+ETO; •). (c) Fatty acid oxidation was determined as 3H2O production when cells were incubated with [9,10-3H]palmitate for 6 h. LN229 cells expressing myrAkt were maintained in serum-free medium for 24 h, then cells were shifted to glucose-free medium containing 1 mM AICAR (−glc+AICAR), or 1 mM AICAR in the presence of 60 μ M etomoxir (−glc+AICAR+ETO). (d) Fatty acid oxidation measured as 3H2O production by cells expressing myrAkt when incubated with [9,10-3H]palmitate for 6 h. Cells were cultured in serum-free medium for 24 h, shifted to glucose-free conditions with no drug (−glc), or in the presence of 1 mM bezafibrate (−glc+BEZA). (e) Percent viability was measured by propidium iodide exclusion for myrAkt-expressing cells that were plated in serum-free medium for 24 h and then shifted to glucose-free medium with no drug (−glc; ), or treated with 1 mM bezafibrate (−glc+BEZA; •). Data are presented as mean±s.d. of triplicate samples and are representative of three independent experiments

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