GSE160946
FCN3 functions as a tumor suppressor of lung adenocarcinoma through induction of endoplasmic reticulum stress
In this study, we report a novel function of FCN3 (Ficolin 3), a secreted lectin capable of activating the complement pathway, as a tumor suppressor of lung adenocarcinoma (LUAD). First, the expression of FCN3 was strongly down-regulated in cancer tissues compared to matched normal lung tissues, and down-regulation of FCN3 was shown to be significantly correlated with increased mortality among LUAD patients. Interestingly, while ectopic expression of FCN3 led to cell cycle arrest and apoptosis in A549 and H23 cells derived from LUAD, the secreted form of the protein had no effect on the cells. Rather, we found evidence indicating that activation of the unfolded protein response is induced from ectopic expression of FCN3 which lead to endoplasmic reticulum (ER) stress. Consistently, inhibition of ER stress response led enhanced survival of the LUAD cells. Collectively, our data indicate that FCN3 is a tumor suppressor gene functioning through induction of ER stress. Overall design: Examination of transcriptome on control and FCN3 overexpressed lung cancer cell lines by deep sequencing