Calreticulin promotes EMT in pancreatic cancer via mediating Ca²⁺ dependent acute and chronic endoplasmic reticulum stress.

ABSTRACT:

Background

Our previous study showed that calreticulin (CRT) promoted EGF-induced epithelial-mesenchymal transition (EMT) in pancreatic cancer (PC) via Integrin/EGFR-ERK/MAPK signaling. We next investigated the novel signal pathway and molecular mechanism involving the oncogenic role of CRT in PC.

Methods

We investigated the potential role and mechanism of CRT in regulating intracellular free Ca²⁺ dependent acute and chronic endoplasmic reticulum stress (ERS)-induced EMT in PC in vitro and vivo.

Results

Thapsigargin (TG) induced acute ERS via increasing intracellular free Ca²⁺ in PC cells, which was reversed by CRT silencing. Additionally, CRT silencing inhibited TG-induced EMT in vitro by reversing TG-induced changes of the key proteins in EMT s

SUBMITTER: Sheng W 

PROVIDER: S-EPMC7542892 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature