Apoptosis: controlled demolition at the cellular level

Taylor, Rebecca C.; Cullen, Sean P.; Martin, Séamus J.

doi:10.1038/nrm2312

Cited by 2,157 publications

(1,913 citation statements)

References 102 publications

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“…Caspase protease activity is essential for the morphological and biochemical hallmarks of apoptosis 8 . In broad terms, caspases can be activated through one of two pathways -the extrinsic (also called deathreceptor) pathway and the intrinsic (also called mitochondrial) pathway ( Figure 1).…”

Section: Apoptotic Signaling Pathwaysmentioning

confidence: 99%

“…As the name implies, the extrinsic pathway requires external stimulation, this occurs via a death receptor-family member, such as TRAIL-R1 (DR4), TRAIL-R2 (DR5), CD95 (FAS) or TNF-R1, located at the plasma membrane. Following ligand binding, death receptors activate caspases leading to widespread substrate protein cleavage and rapid cell death 8 .…”

Section: Apoptotic Signaling Pathwaysmentioning

confidence: 99%

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A fate worse than death: apoptosis as an oncogenic process

2016

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Section: Apoptotic Signaling Pathwaysmentioning

confidence: 99%

Section: Apoptotic Signaling Pathwaysmentioning

confidence: 99%

A fate worse than death: apoptosis as an oncogenic process

2016

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“…Anoikis due to the intrinsic pathway is mainly initiated by Bim, although a role has been proposed also for Bid [14]. Bim is activated following detachment of cells from the ECM and rapidly promotes the assembly of Bax-Bak oligomers within the OMM [15,16]. Bim is sequestered in the dynein complex and actin filaments until the loss of integrin engagement induces its release and translocation to the mitochondria, where it interacts with Bcl-XL, neutralizing its pro-survival function [17].…”

Section: Intrinsic Pathwaymentioning

confidence: 99%

“…Indeed, they are unable to directly activate Bax and Bak oligomerization, but contribute to cell death by competing for the binding to Bcl-2 of apoptotic activators [22,23]. Bcl-2 is the master anti-apoptotic member of the family, and prevents apoptosis by maintaining mitochondrial membrane integrity [3,16,24,25]. Bcl-2 inhibits apoptosis by heterodimerization with Bad/Bax apoptotic members and preventing their clustering into pores, or sequestering Bim apoptotic activators [21,26].…”

Section: Intrinsic Pathwaymentioning

confidence: 99%

Anoikis: an emerging hallmark in health and diseases

Taddei

Giannoni

Fiaschi

et al. 2011

The Journal of Pathology

452

336

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Anoikis is a programmed cell death occurring upon cell detachment from the correct extracellular matrix, thus disrupting integrin ligation. It is a critical mechanism in preventing dysplastic cell growth or attachment to an inappropriate matrix. Anoikis prevents detached epithelial cells from colonizing elsewhere and is thus essential for tissue homeostasis and development. As anchorage-independent growth and epithelial-mesenchymal transition, two features associated with anoikis resistance, are crucial steps during tumour progression and metastatic spreading of cancer cells, anoikis deregulation has now evoked particular attention from the scientific community. The aim of this review is to analyse the molecular mechanisms governing both anoikis and anoikis resistance, focusing on their regulation in physiological processes, as well as in several diseases, including metastatic cancers, cardiovascular diseases and diabetes.

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“…Apoptosis is a form of cell death orchestrated by caspases, which are proteases that degrade hundreds of substrates involved in cell homeostasis or in structural functions. When cells die by apoptosis, they are phagocytosed rapidly with no spillage of cytoplasmic content (Taylor et al, 2008). In contrast, necrosis occurs with rupture of the plasma membrane, which promotes inflammation.…”

Section: Glucose Deprivation and Antiglycolytics Induce Cell Cycle Armentioning

confidence: 99%

Sugar-free approaches to cancer cell killing

et al. 2010

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Tumors show an increased rate of glucose uptake and utilization. For this reason, glucose analogs are used to visualize tumors by the positron emission tomography technique, and inhibitors of glycolytic metabolism are being tested in clinical trials. Upregulation of glycolysis confers several advantages to tumor cells: it promotes tumor growth and has also been shown to interfere with cell death at multiple levels. Enforcement of glycolysis inhibits apoptosis induced by cytokine deprivation. Conversely, antiglycolytic agents enhance cell death induced by radio-and chemotherapy. Synergistic effects are likely due to regulation of the apoptotic machinery, as glucose regulates activation and levels of proapoptotic BH3-only proteins such as Bim, Bad, Puma and Noxa, as well as the antiapoptotic Bcl-2 family of proteins. Moreover, inhibition of glucose metabolism sensitizes cells to death ligands. Glucose deprivation and antiglycolytic drugs induce tumor cell death, which can proceed through necrosis or through mitochondrial or caspase-8-mediated apoptosis. We will discuss how oncogenic pathways involved in metabolic stress signaling, such as p53, AMPK (adenosine monophosphate-activated protein kinase) and Akt/mTOR (mammalian target of rapamycin), influence sensitivity to inhibition of glucose metabolism. Finally, we will analyze the rationale for the use of antiglycolytic inhibitors in the clinic, either as single agents or as a part of combination therapies.

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Apoptosis: controlled demolition at the cellular level

Cited by 2,157 publications

References 102 publications

A fate worse than death: apoptosis as an oncogenic process

A fate worse than death: apoptosis as an oncogenic process

Anoikis: an emerging hallmark in health and diseases

Sugar-free approaches to cancer cell killing

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