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

ABSTRACT: Pancreatic cancer is one of the most aggressive tumors and patients have 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 using a real-time cell analysis system. Moreover, the in vivo antitumor effect of fisetin was verified in pancreatic cancer using a luciferase-expressing murine xenograft pancreatic cancer model. We found that the AMPK/mTOR signaling pathway was enhanced after fisetin treatment; however, autophagy was not diminished by addin

SUBMITTER: Jia S 

PROVIDER: S-EPMC6374379 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature