Figure 1 | Oncogene

Figure 1

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

Figure 1

AICAR activates AMPK and rescues Akt-expressing cells from death induced by glucose withdrawal. (a) Akt-transformed glioblastoma cells (LN18) and (b) non-Akt-transformed cells (LN229) were plated at 2 × 105 cells/well in serum-free medium in the presence of glucose (+glc; □), or in the absence of glucose with no drug (−glc; ) or with 1 mM AICAR (−glc+AICAR; •). Viability was determined by propidium iodide exclusion at the indicated times. (c) Total cell extracts were assayed by Western blot for phospho-Ser473 Akt (pS473-Akt), phospho-Ser79 ACC (pS79-ACC), phospho-Thr172 AMPK (pT172-AMPK) and actin. Lysates were prepared from cells cultured in serum-free medium in the presence or absence of glucose, with or without 1 mM AICAR for 8 h. (d) Viability of LN229 expressing myrAkt (LN229+Akt) cells was measured when cells were cultured in serum-free medium in the presence of glucose (+glc; □), or in the absence of glucose with no drug (−glc; ) or with 1 mM AICAR (−glc+AICAR; •). (e) LN18 cells were transfected with Akt siRNA (siRNA-Akt) or control siRNA (control). Viability, measured by propidium iodide exclusion, and Western blot for total Akt are shown. Data are presented as mean±s.d. of triplicate samples and are representative of three independent experiments