Autophagy in Cell Life and Cell Death

Anding, Allyson L.; Baehrecke, Eric H.

doi:10.1016/bs.ctdb.2015.07.012

Cited by 143 publications

(108 citation statements)

References 120 publications

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“…The results of the present study also demonstrated that CTD had a similar effect in promoting the apoptosis of NSCLC cells, by detecting levels of apoptotic markers, including anti-apoptosis protein Bcl-2 and pro-apoptosis proteins like Bax and active caspase-3. Based on the background that autophagy is a survival-promoting process that captures, degrades, and recycles intracellular constituents in lysosomes and is considered to serve a distinct role in the suppression of tumorigenesis and promotion of mortality (23,24), to investigate the underlying mechanism, autophagy markers were detected, namely, LC3, p62 and Beclin 1. The results revealed that CTD also exhibited an ability to induce autophagy.…”

Section: Discussionmentioning

confidence: 99%

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Liu

et al. 2018

Oncol Lett

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Abstract. Cantharidin (CTD), a component of Mylabris (blister beetle), is a traditional Chinese medicine that exerts an anticancer effect in multiple types of cancer cells. The aim of the present study was to investigate whether CTD exhibited anti-metastatic and inhibitory cell proliferation effects against human non-small cell lung cancer (NSCLC) A549 cells, and the possible underlying mechanism by which this occurs. The results of the present study demonstrated that CTD arrested proliferation, suppressed invasion and migration and induced apoptosis in A549 cells in vitro. Alterations of apoptosis-associated protein levels, including B-cell lymphoma-2 (Bcl-2), Bcl-associated X (Bax) and active caspase-3, were detected. Furthermore, the present study demonstrated that CTD activated autophagy through downregulation of p62 expression and upregulation of microtubule-associated proteins 1A/1B light chain 3B and Beclin-1 expression. Additionally, western blot analysis identified that CTD inhibited the phosphatidylinositol 3-kinase (PI3K)/RAC serine/threonine protein kinase (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway in NSCLC, demonstrating that the levels of phosphorylated (p-)Akt, p-mTOR, phosphorylated ribosomal p70S6 protein kinase (p-p70-S6K) and cyclin D1 were significantly decreased following treatment with CTD. In conclusion, the results of the present study indicated that CTD impeded cell growth and migration by inhibiting PI3K/Akt/mTOR signaling in NSCLC, and promoted autophagy and apoptosis. CTD exhibited anticancer activity against NSCLC in vitro, revealing it as a potential candidate for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Liu

et al. 2018

Oncol Lett

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“…However, researchers agree that, since it is often difficult to distinguish whether autophagy is a causal or an auxiliary phenomenon of cell death, the line between "cell death by autophagy" and "cell death with autophagy" must be drawn as clearly as possible in functional studies [99], [100]. There are excellent reviews available that deal in greater depth with this condition-specific duality of the pathway [12], [101].…”

Section: Functional Conservation Of the Caspase-autophagy Cross-regulmentioning

confidence: 99%

“…"Autophagic cell death" (ACD), also known as type-II PCD, refers to a particular phenotype of cellular demise whereupon an overabundance of autophagic vesicles is evident in dying cells, giving them a characteristic vacuolated appearance [12], [98]. However, researchers agree that, since it is often difficult to distinguish whether autophagy is a causal or an auxiliary phenomenon of cell death, the line between "cell death by autophagy" and "cell death with autophagy" must be drawn as clearly as possible in functional studies [99], [100].…”

Section: Functional Conservation Of the Caspase-autophagy Cross-regulmentioning

confidence: 99%

Caspase involvement in autophagy

2017

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Caspases are a family of cysteine proteases widely known as the principal mediators of the apoptotic cell death response, but considerably less so as the contributors to the regulation of pathways outside cellular demise. In regards to autophagy, the modulatory roles of caspases have only recently begun to be adequately described. In contrast to apoptosis, autophagy promotes cell survival by providing energy and nutrients through the lysosomal degradation of cytoplasmic constituents. Under basal conditions autophagy and apoptosis cross-regulate each other through an elaborate network of interconnections which also includes the interplay between autophagyrelated proteins (ATGs) and caspases. In this review we focus on the effects of this crosstalk at the cellular level, as we aim to concentrate the main observations from research conducted so far on the fine-tuning of autophagy by caspases. Several members of this protease-family have been found to directly interact with key ATGs involved in different tiers across the autophagic cascade. Therefore, we firstly outline the core mechanism of macroautophagy in brief. In an effort to emphasize the importance of the intricate cross-regulation of ATGs and caspases, we also present examples drawn from Drosophila and plant models regarding the contribution of autophagy to apoptotic cell death during normal development. Keywords and abbreviationsautophagy; macroautophagy; mammals; caspases; apoptosis; crosstalk; regulation AMBRA-1Activating-molecule-in-Beclin1-regulated-autophagy-1 AMPK AMP-activated-protein-kinase ATG Autophagy-related gene ATG14L ATG14-likeBcl-2 B-cell lymphoma 2 • Autophagy is implicated in many physiological and pathological processes, where apoptosis is also involved DISC Death-inducing signalling complex FADD Fas-associated protein with death domain Open Questions• Does control of autophagy by caspases represent a central or a supplementary mode of regulation of this pathway?• Is caspase activation required to control autophagy?• To what extent do caspases affect autophagy and how exactly their effects on the pathway vary across different contexts?4

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“…In most physiological settings, autophagy functions as a cell survival mechanism by degrading cellular components to generate energy or macromolecular building blocks for the cells (Anding & Baehrecke 2015). Thus, autophagy defect may promote cell death and decrease the cell number in the heart, which disrupts normal cardiac development.…”

Section: Cell Deathmentioning

confidence: 99%

Autophagy in Cardiac Development

Zhu

2017

MRAJ

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The heart is the first functional organ to form during embryogenesis. Cardiac development is a multifactorial complex process requiring precise control of proliferation, differentiation, migration and survival of diverse cell types by interactive networks of genetic and environmental factors. Autophagy is a conserved catabolic pathway that degrades cytoplasmic contents in lysosomes for reutilization. It is well established that autophagy regulates the development of the nervous system, osseous tissue, adipose tissue and lymphocyte. Recent evidences on the basis of in vitro cell culture systems as well as in vivo animal models suggest essential roles of autophagy in cardiogenesis. In this review, we summarize the major findings regarding emerging roles of autophagy and autophagyrelated genes in cardiac development, which implicates autophagy in human congenital heart disease, the leading human birth defect worldwide.

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Autophagy in Cell Life and Cell Death

Cited by 143 publications

References 120 publications

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Caspase involvement in autophagy

Autophagy in Cardiac Development

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