FADD at the Crossroads between Cancer and Inflammation

Mouasni, Sara; Tourneur, Léa

doi:10.1016/j.it.2018.10.005

Cited by 64 publications

(64 citation statements)

References 101 publications

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“…FADD was originally described as an adapter molecule for apoptosis and is the key to transmitting death signals from cell surface receptors (Mouasni & Tourneur, 2018). It is closely related to autophagic cell death and tumor development.…”

Section: Discussionmentioning

confidence: 99%

“…Zhu et al (2020), PeerJ, DOI 10.7717/peerj.8288 Kischkel et al, 1995)/ apoptosis (Mouasni & Tourneur, 2018)/ interaction with ATG5 (Pyo et al, 2005)/ a negative regulator of necroptosis (Osborn et al, 2010) regulate cell cycle progression and proliferation a cancer driver in oral, esophageal, laryngeal, and breast carcinomas (Callegari et al, 2016;Chien et al, 2016;Prapinjumrune et al, 2010)/ a marker for predicting prognosis in NSCLC (Cimino et al, 2012) Notes. EIF4E, eukaryotic translation initiation factor 4E; mTOR, mammalian target of rapamycin; SCC, squamous cell carcinomas; TIGAR, TP53-induced glycolysis and apoptosis regulator; HK II, hexokinase II; PGM, phosphoglycerate mutase; ROS, reactive oxygen species; OS, overall survival; NSCLC, Non-small-cell lung cancer; FAICAR, formyl-5-Aminoimidazole-4-carboxa-mide-1-β-Dribofuranoside; IMP, inositol monophosphate; HCC, hepatocellular carcinoma; PDI, protein disulfide isomerase; DRs, death receptors; ATG5, autophagy-related 5. thought of autophagy pattern can further develop our study and provide the internal mechanisms of autophagy-related network.…”

Section: Discussionmentioning

confidence: 99%

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Development of an autophagy-related gene prognostic signature in lung adenocarcinoma and lung squamous cell carcinoma

Zhu

Wang

2020

PeerJ

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Purpose There is plenty of evidence showing that autophagy plays an important role in the biological process of cancer. The purpose of this study was to establish a novel autophagy-related prognostic marker for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Methods The mRNA microarray and clinical data in The Cancer Genome Atlas (TCGA) were analyzed by using a univariate Cox proportional regression model to select candidate autophagy-related prognostic genes. Bioinformatics analysis of gene function using the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) platforms was performed. A multivariate Cox proportional regression model helped to develop a prognostic signature from the pool of candidate genes. On the basis of this prognostic signature, we could divide LUAD and LUSC patients into high-risk and low-risk groups. Further survival analysis demonstrated that high-risk patients had significantly shorter disease-free survival (DFS) than low-risk patients. The signature which contains six autophagy-related genes (EIF4EBP1, TP63, BNIP3, ATIC, ERO1A and FADD) showed good performance for predicting the survival of LUAD and LUSC patients by having a better Area Under Curves (AUC) than other clinical parameters. Its efficacy was also validated by data from the Gene Expression Omnibus (GEO) database. Conclusion Collectively, the prognostic signature we proposed is a promising biomarker for monitoring the outcomes of LUAD and LUSC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Development of an autophagy-related gene prognostic signature in lung adenocarcinoma and lung squamous cell carcinoma

Zhu

Wang

2020

PeerJ

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“…FADD is a critical adaptor protein that transmits apoptosis signals by interacting with cell-surface death receptors (DRs) and recruiting caspase-8. Recent studies have indicated that FADD expression is correlated with tumor development (35). FADD expression was previously found to be significantly increased in LUAD and was associated with a poor prognosis (36).…”

Section: Discussionmentioning

confidence: 99%

Ceramide Pathway Regulators Predict Clinical Prognostic Risk and Affect the Tumor Immune Microenvironment in Lung Adenocarcinoma

et al. 2020

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The ceramide pathway is strongly associated with the regulation of tumor proliferation, differentiation, senescence, and apoptosis. This study aimed to explore the gene signatures, prognostic value, and immune-related effects of ceramide-regulated genes in lung adenocarcinoma (LUAD). Methods: Public datasets of LUAD from The Cancer Genome Atlas and Gene Expression Omnibus were selected. Consensus clustering was adopted to classify LUAD patients, and a least absolute shrinkage and selection operator (LASSO) regression model was employed to develop a prognostic risk signature. CIBERSORT algorithm was used to estimate the association between the risk signature and the tumor immune microenvironment. Results: Most of the 22 ceramide-regulated genes were differentially expressed between LUAD and normal samples. LUAD patients were classified into two subgroups (cluster 1 and 2) and cluster 2 was associated with a poor prognosis. Furthermore, a prognostic risk signature was developed based on the three ceramide-regulated genes, Cytochrome C (CYCS), V-rel reticuloendotheliosis viral oncogene homolog A (RELA) and Fas-associated via death domain (FADD). LUAD patients with low-and high-risk scores differed concerning the subtypes of tumor−infiltrating immune cells. A moderate to weak correlation was observed between the risk score and tumor−infiltrating immune cells. Conclusions: Ceramide-regulated genes could predict clinical prognostic risk and affect the tumor immune microenvironment in LUAD.

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“…One of the first reports on the CD95 DISC composition identified two proteins, termed CAP1 and CAP2, that turned out to be phosphorylated FADD forms [8,22]. Later, phosphorylation sites that regulate FADD function and cellular localization were identified at S194 (S191 of murine FADD) [20,23], S200 [24], and S203 [25] (Figure 2A). Phosphorylation of FADD is mediated by a number of kinases, including protein kinase Cζ, antimitotic kinase Aurora-A (Aur-A), casein kinase α (CKIα), casein kinase 2 (CK2), and polo-like kinase 1 (Plk1) [25].…”

Section: Roles For Phosphorylationmentioning

confidence: 98%

“…The proper structural conformation of FADD is a requirement for the initiation of DED filament growth (Box 2). Hence, its modulation by PTM might have major consequences for apoptosis initiation [20]. Several putative PTM sites in FADD DED have been predicted in silico and even identified by mass spectrometry, including phosphorylation and ubiquitylation.…”

mentioning

confidence: 99%

Controlling Cell Death through Post-translational Modifications of DED Proteins

Seyrek

Ivanisenko

Richter

et al. 2020

Trends in Cell Biology

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Apoptosis is a form of programmed cell death, deregulation of which occurs in multiple disorders, including neurodegenerative and autoimmune diseases as well as cancer. The formation of a death-inducing signaling complex (DISC) and death effector domain (DED) filaments are critical for initiation of the extrinsic apoptotic pathway. Post-translational modifications (PTMs) of DED-containing DISC components such as FADD, procaspase-8, and c-FLIP comprise an additional level of apoptosis regulation, which is necessary to overcome the threshold for apoptosis induction. In this review we discuss the influence of PTMs of FADD, procaspase-8, and c-FLIP on DED filament assembly and cell death induction, with a focus on the 3D organization of the DED filament. Death Effector Domain (DED) Proteins in Extrinsic Apoptosis Signaling In multicellular organisms, tissue homeostasis is maintained through a fine-tuned balance between cell proliferation and cell death [1-5]. Several physiological and pathological stimuli have been reported to trigger programmed cell death [6]. Apoptosis can be induced via two pathways: the extrinsic and the intrinsic or mitochondrial pathway [2] (Figure 1). The extrinsic pathway is triggered upon binding of death ligands, including CD95 ligand (CD95L) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) to death receptors (DRs) such as Fas/CD95 and TRAIL receptor-1/2 (TRAILR1/2), respectively [7]. This association leads to the recruitment of proteins with death domains (DD) such as Fas-associated protein with death domain (FADD) to the DD of CD95 or TRAIL-R1/2, resulting in the formation of the death-inducing signaling complex (DISC) [8,9], which in turn directs cleavage and activation of caspases for inducing apoptosis. DISC is comprised of procaspase-8/10 and cellular FLICE-like inhibitory protein (c-FLIP). Upon induction of apoptosis, the DED of FADD interacts with DEDs of procaspase-8, procaspase-10, and c-FLIP, resulting in the formation of DED-filaments, which serve as a platform for procaspase-8 dimerization and subsequent activation [10-12] (Figure 1). DED belongs to the DD superfamily [3,13]. DED comprises six α-helixes arranged in a Greek key structural motif. FADD contains one DD and one DED, whereas both caspase-8 and c-FLIP contain two DEDs at their N terminus. DED filaments are formed through so-called type I, II, and III interactions between DEDs (Box 1) [12]. Proper architecture of DED filaments at DR complexes provide an extra layer of regulatory control of cell death. Recent findings are revealing a role for post-translational modifications (PTMs) such as phosphorylation, ubiquitylation, SUMOylation, and nitrosylation in regulating these interactions [6,14-17]. These modifications assist in maintaining proper conformations of DEDs in DED filaments, which is required for efficient caspase-8 activation, and in overcoming a threshold for apoptosis induction [18,19]. In this review, we consider the role of PTMs in controlling the mechanisms of DISC and DED filament...

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FADD at the Crossroads between Cancer and Inflammation

Cited by 64 publications

References 101 publications

Development of an autophagy-related gene prognostic signature in lung adenocarcinoma and lung squamous cell carcinoma

Development of an autophagy-related gene prognostic signature in lung adenocarcinoma and lung squamous cell carcinoma

Ceramide Pathway Regulators Predict Clinical Prognostic Risk and Affect the Tumor Immune Microenvironment in Lung Adenocarcinoma

Controlling Cell Death through Post-translational Modifications of DED Proteins

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