CD95-mediated cell signaling in cancer: mutations and post-translational modulations

Tauzin, Sébastien; Debure, Laure; Moreau, Jean-François; Legembre, Patrick

doi:10.1007/s00018-011-0866-4

Cited by 47 publications

(45 citation statements)

References 113 publications

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“…CD95L is a transmembrane "cytokine" whose extracellular domain can be cleaved by metalloproteases (2), to produce a soluble ligand. This soluble form was initially described as an inert ligand that competes with its membranebound counterpart for binding to CD95, thus acting as an antagonist of the death signal (3,4).…”

Section: Introductionmentioning

confidence: 99%

CD95L Cell Surface Cleavage Triggers a Prometastatic Signaling Pathway in Triple-Negative Breast Cancer

et al. 2013

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Triple-negative breast cancers (TNBC) lacking estrogen and progesterone receptors and HER2 amplification have a relatively high risk of metastatic dissemination, but the mechanistic basis for this risk is not understood. Here, we report that serum levels of CD95 ligand (CD95L) are higher in patients with TNBC than in other patients with breast cancer. Metalloprotease-mediated cleavage of CD95L expressed by endothelial cells surrounding tumors generates a gradient that promotes cell motility due to the formation of an unconventional CD95-containing receptosome called the motility-inducing signaling complex. The formation of this complex was instrumental for Nox3-driven reactive oxygen species generation. Mechanistic investigations revealed a YesOrai1-EGFR-PI3K pathway that triggered migration of TNBC cells exposed to CD95L. Our findings establish a prometastatic function for metalloprotease-cleaved CD95L in TNBCs, revisiting its role in carcinogenesis. Cancer Res; 73(22); 6711-21. Ó2013 AACR.

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Section: Introductionmentioning

confidence: 99%

CD95L Cell Surface Cleavage Triggers a Prometastatic Signaling Pathway in Triple-Negative Breast Cancer

et al. 2013

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“…After activation of these caspases via auto-cleavage, they are released in the cytosol as active caspases resulting in the apoptotic cell death. The complex CD95/FADD/caspase-8/-10 is called DISC stands for Bdeath-inducing signaling complex^ [96].…”

Section: Fas Cell Surface Death Receptor and Fas Ligandmentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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“…Membrane-bound CD95L (memCD95L) can be processed in its stalk region by various proteases, including matrix metalloproteinase-3 (MMP3), MMP7, MMP9, and a distintegrin and metalloproteinase-10 (ADAM10), leading to the release of soluble CD95L (sCD95L) molecules (Matsuno et al, 2001;Mitsiades et al, 2001;Vargo-Gogola et al, 2002;Kirkin et al, 2007;Schulte et al, 2007). Soluble CD95L still contains the TNF homology domain and therefore retains the homotrimeric structure of the membrane-bound precursor molecule and the ability to interact with CD95 (Tauzin et al, 2012). Biochemical evidence and molecular modeling suggest that CD95L, like other ligands of the TNF family for which the X-ray structure of the ligand-receptor complex has been solved, interacts with three molecules of its receptor CD95 (Sessler et al, 2013).…”

Section: Cd95l-cd95 Interactionmentioning

confidence: 98%

Principles and mechanisms of CD95 activation

Wajant

2014

Biological Chemistry

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CD95 (Apo1/Fas) has been originally identified as the target of cell death-inducing antibodies. The recognition of CD95 as an apoptosis-triggering receptor represents one of the early milestones in the apoptosis field. Moreover, the research on CD95-induced cell death fostered various other discoveries of broad and general relevance in cell biology, for example, the identification of caspase 8 as the initiator caspase of the extrinsic apoptosis pathway. Activation of CD95-associated intracellular signaling pathways is not a simple consequence of ligand binding but is the fine-tuned result of a complex interplay of various molecular mechanisms that eventually determine the strength and quality of the CD95 response. There is growing evidence that different forms of CD95 stimulation trigger the assembly of CD95 signaling complexes of distinct composition. Moreover, the formation of signaling competent CD95 complexes is a multistep process and the subject of regulation by various cellular cues. This review addresses the relevance of the molecular nature of the CD95-stimulating agonist for the quality of the CD95 response and discusses the importance of modification, clustering, internalization, and lipid raft and actin association of CD95 for CD95 activity.

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CD95-mediated cell signaling in cancer: mutations and post-translational modulations

Cited by 47 publications

References 113 publications

CD95L Cell Surface Cleavage Triggers a Prometastatic Signaling Pathway in Triple-Negative Breast Cancer

CD95L Cell Surface Cleavage Triggers a Prometastatic Signaling Pathway in Triple-Negative Breast Cancer

Major apoptotic mechanisms and genes involved in apoptosis

Principles and mechanisms of CD95 activation

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