Fig. 4: nhibition of AMPK/mTOR signaling did not markedly alleviate the autophagy induced by fisetin. | Cell Death & Disease

Fig. 4: nhibition of AMPK/mTOR signaling did not markedly alleviate the autophagy induced by fisetin.

From: Fisetin induces autophagy in pancreatic cancer cells via endoplasmic reticulum stress- and mitochondrial stress-dependent pathways

Fig. 4

I Cells were treated as described previously. a Western blot detection of the expression of PINK1 and Parkin, both which were involved in mitochondrial stress-mediated autophagy. b Western blot detection of the expression of PERK, ATF4, and ATF6, both of which were involved in endoplasmic reticulum (ER) stress-mediated autophagy. c Expressions of ATF4, ATF6, Parkin, LC3B in control and fisetin treatemt groups of mice were examined by immunohistochemistry. Bar scale 50 μm. d, e Mitophagy were examined by colocalization analysis of LC3B and Tom20 (a marker of mitochondria). Yellow spots suggested that mitophagy was increased by fisetin. ***P ≤ 0.001. f, g To inhibit AMPK/mTOR signaling pathway, cells were treated with AMPK inhibitor compound C (CC) (20 μM)for 4 h before collection. Western blot detection showed that expression of PINK1 and Parkin were reduced by CC. However, the expression of PERK, ATF4, ATF6 were not blocked by CC, even the level of ATF4 was increased

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