Regression of apoptosis-resistant colorectal tumors by induction of necroptosis in mice

He, Gui-Wei; Günther, Claudia; Thonn, Veronika; Yu, Yuqiang; Martini, Eva; Buchen, Barbara; Neurath, Markus F.; Stürzl, Michael; Becker, Christoph

doi:10.1084/jem.20160442

Cited by 66 publications

(54 citation statements)

References 23 publications

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“…Recently, He et al . have demonstrated in both a genetic and a xenograft mouse model that induction of necroptosis is a plausible strategy for overcoming cell death resistance in caspase‐8 deficient colorectal cancer.…”

Section: Are Necroptotic Cancer Cells Immunogenic?mentioning

confidence: 99%

“…Recently, He et al 44 Initial work showed that necroptotic fibrosarcoma L929 cells subjected to TNF-induced necroptosis do not induce pro-inflammatory cytokine production in macrophages in vitro. 45 Similarly, B16 mouse melanoma cells in which necroptosis was triggered by over-expression of FADD-death domain were unable to induce maturation of dendritic cells.…”

Section: Are Necroptotic Cancer Cells Immunogenic?mentioning

confidence: 99%

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Necroptotic cell death in anti‐cancer therapy

Krysko

Aaes

Kagan

et al. 2017

Immunological Reviews

141

103

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Necroptosis is one the best-characterized forms of regulated necrosis. Necroptosis is mediated by the kinase activities of receptor interacting protein kinase-1 and receptor interacting protein kinase-3, which eventually lead to the activation of mixed lineage kinase domain-like. Necroptosis is characterized by rapid permeabilization of the plasma membrane, which is associated with the release of the cell content and subsequent exposure of damage-associated molecular patterns (DAMPs) and cytokines/chemokines. This release underlies the immunogenic nature of necroptotic cancer cells and their ability to induce efficient anti-tumor immunity. Triggering necroptosis has become especially important in experimental cancer treatments as an alternative to triggering apoptosis because one of the hallmarks of cancer is the blockade or evasion of apoptosis. In this review, we discuss recent advances in necroptosis research and the functional consequences of necroptotic cancer cell death, with focus on its immunogenicity and its role in the activation of anti-tumor immunity. Next, we discuss the molecular mechanisms of phosphatidylserine exposure during necroptosis and its role in the recognition of necroptotic cells. We also highlight the complex role of the necroptotic pathway in tumor promotion and suppression and in metastasis. Future studies will show whether necroptosis is truly a better strategy to overcome apoptosis resistance and provide the insights needed for development of novel treatment strategies for cancer.

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Section: Are Necroptotic Cancer Cells Immunogenic?mentioning

confidence: 99%

Section: Are Necroptotic Cancer Cells Immunogenic?mentioning

confidence: 99%

Necroptotic cell death in anti‐cancer therapy

Krysko

Aaes

Kagan

et al. 2017

Immunological Reviews

141

103

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“…Earlier studies showed that, in apoptosis-resistant leukemia cells, SMs can potentiate TNF-induced necroptosis by enhancing the formation of the necrosome complex [84,115]. Subsequently, SM treatment induced massive cell death and led to regression of tumors in solid tumors [116,117]. These findings indicated that SMs can combine with death receptors to trigger apoptotic cell death.…”

Section: Combined With Death-inducing Ligandsmentioning

confidence: 93%

Potency and Selectivity of SMAC/DIABLO Mimetics in Solid Tumor Therapy

Zhao

Wang

Wei

et al. 2020

Cells

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Aiming to promote cancer cell apoptosis is a mainstream strategy of cancer therapy. The second mitochondria-derived activator of caspase (SMAC)/direct inhibitor of apoptosis protein (IAP)-binding protein with low pI (DIABLO) protein is an essential and endogenous antagonist of inhibitor of apoptosis proteins (IAPs). SMAC mimetics (SMs) are a series of synthetically chemical compounds. Via database analysis and literature searching, we summarize the potential mechanisms of endogenous SMAC inefficiency, degradation, mutation, releasing blockage, and depression. We review the development of SMs, as well as preclinical and clinical outcomes of SMs in solid tumor treatment, and we analyze their strengths, weaknesses, opportunities, and threats from our point of view. We also highlight several questions in need of further investigation.

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“…For example, mutations in Casp8 were observed in ~30% of the hypermutated colorectal cancer (CRC) samples (64). He et al directly tested the consequences of necroptosis in these cells by crossing ApcMin/+ CRCprone mice to intestinal epithelium-deleted Casp8 -/-mice (Casp8ΔIEC) (64) or by using xenografts of HT29 cells with CRISPR-deleted Casp8. In both cases, unbridled activation of RIPK1 following administration of a clinical SMAC mimetic LCL161 led to massive activation of cell death in vivo, presumably through necroptosis, and tumor regression.…”

Section: Reviewmentioning

confidence: 99%

“…Activation of RIPK1/RIPK3-dependent apoptosis or necroptosis typically requires additional modifiers, such as inhibition of cIAPs for activation of RIPK1 kinase-dependent apoptosis (73,74) and/or inhibition of caspase-8 for RIPK1/RIPK3 kinasedependent necroptosis (64,66,75,76). Consequently, Moriwaki et al examined cell death in response to a panel of commonly used chemotherapeutic agents and did not observe any changes in cell death upon knockdown of either RIPK1 or RIPK3 in RIPK3-expressing cells or upon overexpression of RIPK3 in cells that lost RIPK3 expression(37), suggesting that RIPK1/RIPK3 may not be generally involved in chemotherapy-induced cell death.…”

Section: Roles Of Ripk1/ripk3 In Immunogenic Cell Death Responses Tomentioning

confidence: 99%