Flightless-1 inhibits ER stress-induced apoptosis in colorectal cancer cells by regulating Ca²⁺ homeostasis.

ABSTRACT: The endoplasmic reticulum (ER) stress response is an adaptive mechanism that is activated upon disruption of ER homeostasis and protects the cells against certain harmful environmental stimuli. However, critical and prolonged cell stress triggers cell death. In this study, we demonstrate that Flightless-1 (FliI) regulates ER stress-induced apoptosis in colon cancer cells by modulating Ca²⁺ homeostasis. FliI was highly expressed in both colon cell lines and colorectal cancer mouse models. In a mouse xenograft model using CT26 mouse colorectal cancer cells, tumor formation was slowed due to elevated levels of apoptosis in FliI-knockdown (FliI-KD) cells. FliI-KD cells treated with ER stress inducers, thapsigargin (TG), and tunicamycin exhibited activation of the unfolded protein re

SUBMITTER: Choi SS 

PROVIDER: S-EPMC7338537 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature