Inhibition of autophagy abrogates tumour necrosis factor α induced apoptosis in human T‐lymphoblastic leukaemic cells

Li, Jia; Dourmashkin, R. R.; Allen, Paul D.; Gray, A.; Newland, Adrian C.; Kelsey, Stephen M.

doi:10.1046/j.1365-2141.1997.2623081.x

Cited by 211 publications

(161 citation statements)

References 32 publications

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“…77 TNFa, another member of the apoptosis-inducing family, stimulates autophagy and apoptosis in T-lymphoblastic leukemia cells. 78 Inhibition of autophagy by 3-MA protects these cells against death. In addition, TNFa stimulates autophagic cell death independently of caspase activation.…”

Section: Other Signaling Pathways Activated During Autophagic Cell Deathmentioning

confidence: 99%

Autophagy and signaling: their role in cell survival and cell death

2005

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Macroautophagy is a vacuolar, self-digesting mechanism responsible for the removal of long-lived proteins and damaged organelles by the lysosome. The discovery of the ATG genes has provided key information about the formation of the autophagosome, and about the role of macroautophagy in allowing cells to survive during nutrient depletion and/or in the absence of growth factors. Two connected signaling pathways encompassing class-I phosphatidylinositol 3-kinase and (mammalian) target of rapamycin play a central role in controlling macroautophagy in response to starvation. However, a considerable body of literature reports that macroautophagy is also a cell death mechanism that can occur either in the absence of detectable signs of apoptosis (via autophagic cell death) or concomitantly with apoptosis. Macroautophagy is activated by signaling pathways that also control apoptosis. The aim of this review is to discuss the signaling pathways that control macroautophagy during cell survival and cell death.

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Section: Other Signaling Pathways Activated During Autophagic Cell Deathmentioning

confidence: 99%

Autophagy and signaling: their role in cell survival and cell death

2005

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“…2,[16][17][18] The recent association of autophagic cell death with models of tumorigenesis [19][20][21][22] and neurodegenerative disorders [23][24][25][26] has led to greater interest in the mechanisms that regulate this form of cell destruction.…”

Section: Introductionmentioning

confidence: 99%

Autophagic programmed cell death in Drosophila

2003

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Autophagic programmed cell death occurs during the development of diverse animal groups, but the mechanisms that control this genetically regulated form of cell killing are poorly understood. Genetic studies of bulk protein degradation in yeast have provided important advances in our understanding of autophagy, and recent investigations of Drosophila autophagic cell death suggest that some of these mechanisms may be conserved. In Drosophila, several steroid-regulated genes that encode transcription regulators are required for autophagic cell death. These transcription regulators appear to activate a large number of genes that play a more direct role in cell killing, including genes that function in apoptosis such as caspases. While caspase function is required for autophagic cell death during Drosophila development, genes encoding proteins that are similar to the yeast autophagy regulators are also induced in dying salivary glands. Furthermore, numerous noncaspase proteases, cytoplasmic organizing factors, signaling molecules, and unknown factors are expressed in interesting patterns during autophagic cell death. This article reviews the current knowledge of the regulation of autophagic programmed cell death during development of Drosophila.

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“…56 More recently, TNFa was found to induce an autophagic type of cell death in Tlymphoblastic leukaemic cells; 3-MA inhibited both the formation of autophagosomes and cell death. 50 However, asparagine, which inhibits the fusion of lysosomes with autophagosomes, did not prevent TNF-a induced cell death. 50 Thus, inhibition of an event downstream of sequestration ( Figure 2) did not affect the execution of autophagic cell death, suggesting that the supply of lysosomes might not be a check point for initiation of this type of programmed cell death.…”

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confidence: 99%

“…50 However, asparagine, which inhibits the fusion of lysosomes with autophagosomes, did not prevent TNF-a induced cell death. 50 Thus, inhibition of an event downstream of sequestration ( Figure 2) did not affect the execution of autophagic cell death, suggesting that the supply of lysosomes might not be a check point for initiation of this type of programmed cell death. Likewise, tamoxifeninduced autophagic cell death in MCF-7 cells was not associated with an expansion of the lysosomal compartment as indicated by biochemical and histochemical means (To È ro È k and Bursch, unpublished observation).…”

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The autophagosomal–lysosomal compartment in programmed cell death

2001

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In the last decade a tremendous progress has been achieved in understanding the control of apoptosis by survival and death factors as well as the molecular mechanisms of preparation and execution of the cell's suicide. However, accumulating evidence suggests that programmed cell death (PCD) is not confined to apoptosis but that cells use different pathways for active self-destruction as reflected by different morphology: condensation prominent, type I or apoptosis; autophagy prominent, type II; etc. Autophagic PCD appears to be a phylogenetically old phenomenon, it may occur in physiological and disease states. Recently, distinct biochemical and molecular features have been be assigned to this type of PCD. However, autophagic and apoptotic PCD should not be considered as mutually exclusive phenomena. Rather, they appear to reflect a high degree of flexibility in a cell's response to changes of environmental conditions, both physiological or pathological. Furthermore, recent data suggest that diverse or relatively unspecific signals such as photodamage or lysosomotropic agents may be mediatd by lysosomal cysteine proteases (cathepsins) to caspases and thus, apoptosis. The present paper reviews morphological, functional and biochemical/molecular data suggesting the participation of the autophagosomal ± lysosomal compartment in programmed cell death. Cell Death and Differentiation (2001) 8, 569 ± 581.

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Inhibition of autophagy abrogates tumour necrosis factor α induced apoptosis in human T‐lymphoblastic leukaemic cells

Cited by 211 publications

References 32 publications

Autophagy and signaling: their role in cell survival and cell death

Autophagy and signaling: their role in cell survival and cell death

Autophagic programmed cell death in Drosophila

The autophagosomal–lysosomal compartment in programmed cell death

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