GSE117189
Fisetin induces autophagy in pancreatic cancer cells via endoplasmic reticulum stress- and mitochondrial stress-dependent pathways
Pancreatic cancer is one of the most aggressive tumors and has poor survival rates. Fisetin, a natural flavonoid, was recently reported to have antitumor effects in various cancer models. Autophagy is a conserved catabolic process that maintains cellular homoeostasis in response to stress, and together with apoptosis, determines cell fate. Herein, we examined the effect of fisetin on pancreatic cancer. We reveal that fisetin inhibits Panc-1 cell proliferation in vivo and in vitro. We found that AMPK-dependent autophagy was enhanced after fisetin treatment.However RNA-seq analysis revealed that the unfolded protein response, which is activated by ER stress, was enriched. We also found that there may be crosstalk between the AMPK- and p8-dependent pathways. Overall design: Total mRNA profiles of human pancreatic cancer Panc-1 cells with or without treatment of Fisetin, were generated by deep sequencing, in triplicate.