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FCN3 functions as a tumor suppressor of lung adenocarcinoma through induction of endoplasmic reticulum stress

Title
FCN3 functions as a tumor suppressor of lung adenocarcinoma through induction of endoplasmic reticulum stress
Authors
Jang, HaeyeonJun, YukyungKim, SuyeonKim, EunjeongJung, YeonjooPark, Byung JoLee, JinseonKim, JhingookLee, SanghyukKim, Jaesang
Ewha Authors
이상혁김재상정연주
SCOPUS Author ID
이상혁scopus; 김재상scopus; 정연주scopus
Issue Date
2021
Journal Title
CELL DEATH & DISEASE
ISSN
2041-4889JCR Link
Citation
CELL DEATH & DISEASE vol. 12, no. 4
Publisher
SPRINGERNATURE
Indexed
SCOPUS; SCIE WOS
Document Type
Article
Abstract
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 from endoplasmic reticulum (ER) stress is induced by ectopic expression of FCN3. Consistently, inhibition of ER stress response led to enhanced survival of the LUAD cells. Of note, the fibrinogen domain, which is not secreted, turned out to be both necessary and sufficient for induction of apoptosis when localized to ER, consistent with our proposed mechanism. Collectively, our data indicate that FCN3 is a tumor suppressor gene functioning through induction of ER stress.
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DOI
10.1038/s41419-021-03675-y
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자연과학대학 > 생명과학전공 > Journal papers
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