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TRAIL-induced cancer secretome

ABSTRACT: To comprehensively determine which factors are secreted by cancer cells upon TRAIL stimulation, we conducted an unbiased mass spectrometric analysis of TRAIL’s secretome in resistant A549 cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell Of Lung

DISEASE(S): Non-small Cell Lung Carcinoma

SUBMITTER: Silvia Surinova

LAB HEAD: Silvia Surinova

PROVIDER: PXD005664 | Pride | 2017-12-19

REPOSITORIES: Pride

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			Action	DRS
	Hartwig-et-al.-Table-S1.xlsx	Xlsx
	evidence.txt	Txt
	mqpar.xml	Xml
	msms.txt	Txt
	proteinGroups.txt	Txt

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Publications

The TRAIL-Induced Cancer Secretome Promotes a Tumor-Supportive Immune Microenvironment via CCR2.

Hartwig Torsten T Montinaro Antonella A von Karstedt Silvia S Sevko Alexandra A Surinova Silvia S Chakravarthy Ankur A Taraborrelli Lucia L Draber Peter P Lafont Elodie E Arce Vargas Frederick F El-Bahrawy Mona A MA Quezada Sergio A SA Walczak Henning H

Molecular cell 20170201 4

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known for specifically killing cancer cells, whereas in resistant cancers, TRAIL/TRAIL-R can promote metastasis via Rac1 and PI3K. It remains unknown, however, whether and to what extent TRAIL/TRAIL-R signaling in cancer cells can affect the immune microenvironment. Here we show that TRAIL-triggered cytokine secretion from TRAIL-resistant cancer cells is FADD dependent and identify the TRAIL-induced secretome to drive monoc ...[more]

PMID: 28212753

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Analysis of gene expression in CNOT2-depleted A549 lung cancer cells

Project description:CNOT2 depletion partially decreased number of colony in colony forming assay and cell number in proliferation assay for NSCLC cells. Co-treatment with TRAIL and depletion of CNOT2 dramatically declined survival rate and increased apoptosis compared with TRAIL only in TRAIL resistant NSCLC cells. So, to find major signaling molecules in CNOT2 depleted condition of A549 cells, gene expression analysis was designed.

2019-10-31 | GSE131518 | GEO

Involvement of Mieap in Cardiolipin metabolism (part I)

Project description:Quantitative assessment of total cardiolipin (CL) and comparison of CL species conducted with A549 (Ad-Mieap infected vs. non-infected) and LS174T cells (LS174T-cont vs. Mieap-KD). The A549 cells were harvested 24 hr after infection with Ad-Mieap and were compared with non-infected cells by mass spectrometric analysis. The LS174T-cont and Mieap-KD cells incubated under a normal condition were harvested and subjected to mass spectrometric analysis.

2021-07-30 | ST001893 | MetabolomicsWorkbench

BID is critical for IFN-alpha-induced cell death

Project description:Clinical applications of human interferon (IFN)-alpha have met with varying degrees of success. Nevertheless, key molecules in IFN-alpha-induced cell death have not been clearly identified. Our previous study indicated that IFN (alpha, beta and omega) receptor (IFNAR) 1/2- and IFN regulatory factor (IRF) 9-RNA interference (RNAi) completely inhibited the antiproliferative (AP) activity of IFN-alpha in human ovarian adenocarcinoma OVCAR3 cells sensitive to IFN-alpha., followed by transcription of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Here, IFNAR1/2- and IRF9-RNAi inhibited the gene expression of TRAIL, but not of Fas ligand (FasL), following IFN-alpha treatment. In fact, TRAIL but not FasL inhibited the proliferation of OVCAR3 cells. IFN-alpha notably up-regulated the levels of TRAIL protein in the supernatant and on the membrane of OVCAR3 cells. Following TRAIL signaling, Caspase 8 inhibitor and BH3 interacting domain death agonist (BID)-RNAi significantly abrogated both AP activities of IFN-alpha and TRAIL. Furthermore, BID-RNAi prevented both IFN-alpha and TRAIL from collapsing the mitochondrial membrane potential (Delta Psi m). Finally, we provide important new evidence that BID overexpression led to a major enhancement of both AP activities of IFN-alpha and TRAIL in human lung carcinoma A549 cells resistant to IFN-alpha. Thus, this study suggests that BID is crucial in IFN-alpha-induced cell death, indicating a notable potential to be a targeted therapy for IFN-alpha resistant tumors.

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Involvement of Mieap in Cardiolipin metabolism (part I-revised)

Project description:Cardiolipin (CL) alterations cause mitochondrial dysfunction. Mieap is involved in mitochondrial quality control (MQC). To investigate whether Mieap functions in MQC via regulation of CL metabolism, quantitative assessment of total CL and comparison of CL species conducted with A549 (Ad-Mieap infected vs. non-infected) and LS174T cells (LS174T-cont vs. Mieap-KD). The A549 cells were harvested 24 hr after infection with Ad-Mieap and were compared with non-infected cells by mass spectrometric analysis. The LS174T-cont and Mieap-KD cells incubated under a normal condition were harvested and subjected to mass spectrometric analysis.

2022-02-13 | ST002114 | MetabolomicsWorkbench

BID is critical for IFN-alpha-induced cell death

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TRAIL expressing monocyte/macrophages reduce inflammation and attenuate atherosclerosis

Project description:Circulating TRAIL is reduced in cardiovascular disease patients and TRAIL deletion in mice exacerbates disease. The source of TRAIL and protective mechanism(s) are unclear. Monocyte TRAIL mRNA was reduced from coronary artery disease patients, strikingly associating with reduced plasma TRAIL. A strong inverse correlation between plasma TRAIL and IL-18 was observed, with IL-18 repressing monocyte TRAIL mRNA. In mice, two sources were investigated using bone-marrow (BM) transplants; TRAIL expressed only in BM (BM-TRAIL) or everywhere except BM (parenchymal-TRAIL), vs. whole-body TRAIL ablation (null-TRAIL). BM-TRAIL attenuated macrophage content and atherosclerosis. BM-derived macrophages with TRAIL deletion were more inflammatory, with impaired migration and reduced expression of cholesterol efflux, efferocytosis and nitric oxide-controlling genes. TRAIL expression also reduced islet macrophage content, but only parenchymal-TRAIL islets had improved function. Recombinant TRAIL administration stimulated insulin expression and islet mass. We propose TRAIL maintains monocyte/macrophage homeostasis and limits the progression of atherosclerosis and islet dysfunction.

2019-12-03 | GSE107645 | GEO

Influenza A virus induced proteome changes

Project description:Seasonal epidemics of influenza A virus in the human population are a major cause of severe illness and are of high socio-economic relevance. For the design of effective anti-viral therapies, a detailed knowledge of cellular pathways perturbed by virus infection is critical. We performed comprehensive expression and organellar proteomics experiments using A549, Calu-1 and NCI-H1299 cells to identify new protein targets and cellular pathways affected by influenza A virus.

2018-07-12 | PXD009924 | Pride

Proteomic analysis of TRAIL-induced endogenous RIPK3-dependent necrosome complex

Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a well-known inducer of apoptosis via formation of the primary death-inducing signaling complex (TRAIL-DISC) at the level of membrane death receptors (DR4 and DR5) which recruit successively FADD and caspase-8. TRAIL can also induce necroptosis when caspases are inhibited. Necroptosis is a regulated cell death dependent on the formation of a cytosolic necrosome complex which includes RIPK1, RIPK3 and MLKL proteins. Elucidating the molecular mechanisms involved in TRAIL-induced necroptosis might provide new insights into the TRAIL death signaling pathway. Here, we report the analysis by mass spectrometry of endogenous RIPK3-dependent necrosome complex constituents upon necroptosis induced by TRAIL/z-VAD/Birinapant (TzB) in HT29 cells. Besides characterization of RIPK1, RIPK3, MLKL, FADD, caspase-8, we find TRIM21 as a new constituent of the necrosome complex. Moreover RIPK1, RIPK3, MLKL, P-MLKL, FADD, caspase-8 and TRIM21 are also found associated to the native TRAIL-DISC upon TzB stimulation showing initiation of the necrotic pathway at the level of TRAIL death receptors in HT29 cells. Finally, TRIM21 may positively modulate necroptosis induction by downregulating NF-kB activation.

2021-03-18 | PXD003383 | Pride

Host cell gene expression in Influenza A/WSN/33 (H1N1) infected A549 cells at 10 hour post infection

Project description:We used the microarray data to analyze host cells response on A549 cells infected with A/WSN/33 (H1N1) The A/WSN/33 (H1N1) infected A549 cells were harvested at 10 hpi and RNA extraction was performed using standard protocol as described by Affymetrix. The aim of this experiment is to analyze host response to Influenza A/WSN/33 (H1N1) infection.

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ULK1 regulated phosphosites in mouse and human cells

Project description:(1)In vivo SILAC analyses of mouse embryonic fibroblasts (MEFs, triple labeling) were performed comparing phosphorylation events. ULK1 double knock out MEFs (VC) were compared to double knock out MEFs expressing human ULK1 (RE) in fed (DMEM) and starvation (HBSS) conditions. (2) In vivo SILAC analyses of A549 cells (triple labeling) were performed comparing phosphorylation events (195 raw files labeled ""A549""). A549 cells in fed conditions (DMEM) were compared to starved cells (HBSS) and cells treated with rapamycin (Rapa).

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