Protease Activity of Procaspase-8 Is Essential for Cell Survival by Inhibiting Both Apoptotic and Nonapoptotic Cell Death Dependent on Receptor-interacting Protein Kinase 1 (RIP1) and RIP3

Kikuchi, Mina; Kuroki, Shunsuke; Kayama, Mitsuhiro; Sakaguchi, Shota; Lee, Kyung-Kwon; Yonehara, Shin

doi:10.1074/jbc.m112.419747

Cited by 40 publications

(33 citation statements)

References 45 publications

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“…For instance, in human colon cells, RIP1 and RIP3 were required for autophagy, apoptosis and necroptosis induced by C42 . In addition, RIP1 and RIP3 were reported to be involved in caspase-8 deficiency-induced autophagy and apoptosis (Kikuchi et al, 2012). Consistent with these findings, our results found that both NEC-1 and knockdown of RIP3 prevented activation of ROS-JNKp53 loop, autophagy and cleavage of PARP induced by FTY720.…”

Section: Discussionsupporting

confidence: 91%

FTY720 induces autophagy-related apoptosis and necroptosis in human glioblastoma cells

et al. 2015

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Section: Discussionsupporting

confidence: 91%

FTY720 induces autophagy-related apoptosis and necroptosis in human glioblastoma cells

et al. 2015

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“…Co-stimulation by TNF and zVAD could not induce necroptosis in CLL cells, but knockdown of LEF1 re-sensitized CLL cells to TNF-induced necroptosis, suggesting that the defect in necroptosis correlated with CLL pathogenesis [125]. Similar observations were made in lymphomas from T-cell origin in which loss of RIPK3 signaling supported disease progression possibly as a result of necroptosis blockade [126]. Here, Caspase-8 paradoxically promoted cell survival and also increased cellular growth by virtue of its protease activity [126].…”

Section: Necroptosis Signaling In Hematopoietic Malignanciessupporting

confidence: 54%

“…Similar observations were made in lymphomas from T-cell origin in which loss of RIPK3 signaling supported disease progression possibly as a result of necroptosis blockade [126]. Here, Caspase-8 paradoxically promoted cell survival and also increased cellular growth by virtue of its protease activity [126]. Dissecting a cohort of 458 patients, an increased risk of development of non-Hodgkin lymphoma (NHL) was associated with single-nucleotide polymorphisms (SNPs) in RIPK3.…”

Section: Necroptosis Signaling In Hematopoietic Malignanciesmentioning

confidence: 69%

Necroinflammation emerges as a key regulator of hematopoiesis in health and disease

Jost

Höckendorf

2018

Cell Death Differ

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The hematopoietic system represents an organ system with an exceptional capacity for the production of mature blood cells from a small and mostly quiescent pool of hematopoietic stem cells (HSCs). This extraordinary capacity includes selfrenewal but also the propensity to rapidly respond to extrinsic needs, such as acute infections, severe inflammation, and wound healing. In recent years, it became clear that inflammatory signals such as cytokines, chemokine and danger signals from pathogens (PAMPs) or dying cells (DAMPs) impact on HSCs, shaping their proliferation status, lineage bias, and repopulating ability and subsequently increasing the output of mature effector cells. However, inflammatory danger signals negatively impact on the capacity of HSCs to self-renew and to maintain their stem cell capabilities. This is evidenced in conditions of chronic inflammation where bone marrow failure may originate from HSC exhaustion. Even in hematopoietic cancers, inflammatory signals shape the phenotype of the malignant clone as exemplified by necrosome-dependent inflammation elicited during malignant transformation in acute myeloid leukemia. Accordingly, understanding the contribution of inflammatory signals, and specifically necroinflammation, to HSC integrity, HSC long-term functionality, and malignant transformation has attracted substantial research and clinical interest. In this review, we highlight recent developments and open questions at the interplay between inflammation, regulated necrosis, and HSC biology in the context of blood cell development, acute and chronic inflammation, and hematopoietic cancer.

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“…So far, RIP1 has been implicated in the activation of NADPH oxidase 1 at the TNFR1 complex upon TNFα stimulation in one study using mouse embryonic fibroblasts. 15 RIP3 was repeatedly reported to regulate ROS production, 16,17,26,[42][43][44] which has been linked to its ability to activate key metabolic enzymes, leading to an increase in energy metabolism and subsequently ROS production. 17 Besides RIP1 and RIP3, our data provide genetic evidence showing that the deubiquitinase CYLD is required for BV6/TNFα-induced ROS production, necrosome formation and cell death, as CYLD knockdown inhibits these events.…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species regulate Smac mimetic/TNFα-induced necroptotic signaling and cell death

2015

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Necroptosis represents a key programmed cell death pathway involved in various physiological and pathophysiological conditions. However, the role of reactive oxygen species (ROS) in necroptotic signaling has remained unclear. In the present study, we identify ROS as critical regulators of BV6/tumor necrosis factor-α (TNFα)-induced necroptotic signaling and cell death. We show that BV6/TNFα-induced cell death depends on ROS production, as several ROS scavengers such as butylated hydroxyanisole, N-acetylcysteine, α-tocopherol and ethyl pyruvate significantly rescue cell death. Before cell death, BV6/TNFα-stimulated ROS generation promotes stabilization of the receptor-interacting protein kinase 1 (RIP1)/RIP3 necrosome complex via a potential positive feedback loop, as on the one hand radical scavengers attenuate RIP1/RIP3 necrosome assembly and phosphorylation of mixed lineage kinase domain like (MLKL), but on the other hand silencing of RIP1 or RIP3 reduces ROS production. Although MLKL knockdown effectively decreases BV6/TNFα-induced cell death, it does not affect RIP1/RIP3 interaction and only partly reduces ROS generation. Moreover, the deubiquitinase cylindromatosis (CYLD) promotes BV6/TNFα-induced ROS generation and necrosome assembly even in the presence of BV6, as CYLD silencing attenuates these events. Genetic silencing of phosphoglycerate mutase 5 or dynamin-related protein 1 (Drp1) fails to protect against BV6/TNFα-induced cell death. By demonstrating that ROS are involved in regulating BV6/TNFα-induced necroptotic signaling, our study provides new insights into redox regulation of necroptosis.

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Protease Activity of Procaspase-8 Is Essential for Cell Survival by Inhibiting Both Apoptotic and Nonapoptotic Cell Death Dependent on Receptor-interacting Protein Kinase 1 (RIP1) and RIP3

Cited by 40 publications

References 45 publications

FTY720 induces autophagy-related apoptosis and necroptosis in human glioblastoma cells

FTY720 induces autophagy-related apoptosis and necroptosis in human glioblastoma cells

Necroinflammation emerges as a key regulator of hematopoiesis in health and disease

Reactive oxygen species regulate Smac mimetic/TNFα-induced necroptotic signaling and cell death

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