ArticleCell death & disease2021
FCN3 functions as a tumor suppressor of lung adenocarcinoma through induction of endoplasmic reticulum stress.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- STT3A-mediated FCN3 N-glycosylation promotes Treg cell activation to drive hepatocellular carcinoma progression via Wnt/β-catenin.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Identification of prognostic genes associated with sphingosine-1-phosphate in gastric cancer to construct a risk mode.Translational cancer research · 2025Article
- Identification of Hub Genes in Liver Hepatocellular Carcinoma Based on Weighted Gene Co-expression Network Analysis.Biochemical genetics · 2025Article
- Ficolin-3 Activates Complement and Triggers Necroptosis in Cholangiocarcinoma Cells via the RIPK1/RIPK3/MLKL Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Novel mtDNA methylation-associated prognostic signatures in colorectal cancer.Frontiers in oncology · 2025Article
- Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025Review
- Impact of immunosuppressants on tumor pulmonary metastasis: new insight into transplantation for hepatocellular carcinoma.Cancer biology & medicine · 2024Review
- Ficolin-3 induces apoptosis and suppresses malignant property of hepatocellular carcinoma cells via the complement pathway.Life sciences · 2024Article
- HCCDB v2.0: Decompose Expression Variations by Single-cell RNA-seq and Spatial Transcriptomics in HCC.Genomics, proteomics & bioinformatics · 2024Article
- Ficolin 3 promotes ferroptosis in HCC by downregulating IR/SREBP axis-mediated MUFA synthesis.Journal of experimental & clinical cancer research : CR · 2024Article
- Prognostic correlation between specialized capillary endothelial cells and lung adenocarcinoma.Heliyon · 2024Article
- The Role of Ficolins in Lung Injury.Journal of innate immunity · 2024Review
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Identification of endoplasmic reticulum stress-related signature characterizes the tumor microenvironment and predicts prognosis in lung adenocarcinoma.Scientific reports · 2023Article
- Comprehensive and deep profiling of the plasma proteome with protein corona on zeolite NaY.Journal of pharmaceutical analysis · 2023Article
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- Identification of endoplasmic reticulum stress-related lncRNAs in lung adenocarcinoma by bioinformatics and experimental validation.Annals of medicine · 2023Article
- Loss of ficolin-3 expression is associated with poor prognosis in patients with hepatocellular carcinoma.International journal of medical sciences · 2023Article
- Construction and validation of a prognostic model for lung adenocarcinoma based on endoplasmic reticulum stress-related genes.Scientific reports · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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