Calreticulin promotes thapsigargin induced epithelial mesenchymal transition in pancreatic cancer cells

VernacularTitle:钙网蛋白促进毒胡萝卜素诱导的胰腺癌细胞间质转化
Author: Weiwei SHENG ¹ ; Jingtong TANG ; Rongxian CAO ; Lin CHEN ; Chen TIAN ; Ming DONG
Author Information

1. 中国医科大学附属第一医院胃肠外科,沈阳　110001
Keywords: Pancreatic neoplasms; Calreticulin; Thapsigargin; Epithelial mesenchymal transition
From: Chinese Journal of General Surgery 2022;37(7):524-529
CountryChina
Language:Chinese
Abstract: Objective:To investigate the effect of CRT on thapsigargin (TG)-induced epithelial mesenchymal transition (EMT) of pancreatic cancer (PC) cells.Methods:Immunohistochemistry was used to investigate the differential CRT expression in PC tissues. Western blot (WB) and transwell were used to detect the effect of CRT silencing on TG induced EMT phenotype. Fluro-4/AM and confocal microscopy were used to detect intracellular calcium level in PC cells.Results:CRT was overexpressed in PC tissues ( P<0.01). Overexpression of CRT was positively associated with lymph node metastasis ( P=0.017) and UICC stage ( P=0.021) of PC patients, and negatively associated with E-cadherin expression ( P=0.013). High CRT and low E-cad expression contributed to the poor prognosis of PC patients ( P=0.023). In PC cells, TG induced EMT phenotype was reversed by siRNA-mediated CRT silencing. TG induced EMT was significantly reversed by CRT silencing in vitro. Conclusions:CRT mediates TG induced intracytoplasmic Ca 2+, and ultimately promotes EMT of PC cells.