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. 2018 Mar 29;42(1):359–367. doi: 10.3892/ijmm.2018.3599

Figure 6.

Figure 6

AICAR attenuates PFK15-induced suppression of autophagy and cell viability loss, partly blocking the decrease of p-AMPK. (A) Western blots analyzing the expression levels of p62 and LC3 in RD cells treated with AICAR and PFK15 in the presence or absence of CQ (10 μM). (B) Effect of AICAR (0.5 mM) treatment for 2 or 12 h on AMPK activity in the absence and presence of PFK15 (6 μM), as reflected by the phosphorylation of AMPK. (C) RD cells were treated with PFK15 and AICAR for 24 and 48 h, and cell viability was analyzed by an MTS assay. (D) Colony growth assays were performed in RD cells treated with PFK15 (6 μM) in the absence and presence of AICAR. RD, rhabdomyosarcoma; AMPK, adenosine monophosphate-activated protein kinase; *P<0.05 vs. control and **P<0.01 vs. control. AICAR, 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside; CQ, chloroquine diphosphate salt; LC3, light chain 3; p-, phosphorylated; t-, total; Ctrl, control.