Figure 4 : AICAR or rapamycin treatment counteracts the induction of atrogene expression and modulates autophagic markers in cancer cachexia.

From: Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer

Figure 4

(a) Expression of Atrogin 1 and MuRF1 genes as shown by real-time RT-PCR, in mice that received daily IP treatment with vehicle (—), AICAR (AICAR) or rapamycin (RAPA), for 19 days after C26 implant, compared with control mice (CTR). Values were normalized to Gapdh. ANOVA (F = 10.08; df 3; p < 0.01;F = 7.90; df 3; p < 0.01; for Atrogin 1 and MuRF1, respectively) showed a significant effect of the treatments on ubiquitine-ligase relative expression. (b) Representative immunostaining for p62 on TA muscle of C26-bearing mice in the absence (—) or presence of the treatments indicated, showing an increase in p62 induction in C26-bearing mice. Scale bar = 20 microns. (c) Western blot analysis of LC3bI, LC3bII, p62 and Gapdh expression in the presence of the treatments indicated. The lanes separated by the thin black lines were run at the same time on parallel gels and were, therefore, non-contiguous. (d) Densitometric analyses of Western blot showing LC3bII/LC3bI ratio in mice in the presence of the treatments indicated, compared with control mice (CTR). ANOVA (F = 6.26; df 3; p < 0.01) revealed a significant effect of the treatments on the LC3bII/LC3bI ratio. (e) Densitometric analyses of Western blot showing p62 expression in mice in the presence of the treatments indicated, compared with control mice (CTR). Values were normalized to Gapdh. ANOVA (F = 5.92; df 3; p < 0.008) revealed a significant effect of treatments on p62 protein expression. Data are presented as mean ± SEM. *p < 0.05; **p < 0.005 by Tukey’s HSD test.