Destined to Die: Apoptosis and Pediatric Cancers

Choo, Zhang'e; Loh, Amos Hong Pheng; Chen, Zhi Xiong

doi:10.3390/cancers11111623

Cited by 14 publications

(13 citation statements)

References 187 publications

(217 reference statements)

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“…In contrast, apoptosis is defined as programmed cell death. Under a microscope, apoptosis is characterized by apoptotic bodies, nuclear pyknosis and fragmentation, and an intact cell membrane ( Kerr et al, 1972 ; Choo et al, 2019 ). However, an increasing number of studies have described another form of necrosis that performs as programmed and regulated cell death, named necroptosis.…”

Section: Necroptosismentioning

confidence: 99%

Necroptosis: A Novel Pathway in Neuroinflammation

Jiang

et al. 2021

Front. Pharmacol.

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Neuroinflammation is a complex inflammatory process in the nervous system that is expected to play a significant role in neurological diseases. Necroptosis is a kind of necrosis that triggers innate immune responses by rupturing dead cells and releasing intracellular components; it can be caused by Toll-like receptor (TLR)-3 and TLR-4 agonists, tumor necrosis factor (TNF), certain microbial infections, and T cell receptors. Necroptosis signaling is modulated by receptor-interacting protein kinase (RIPK) 1 when the activity of caspase-8 becomes compromised. Activated death receptors (DRs) cause the activation of RIPK1 and the RIPK1 kinase activity-dependent formation of an RIPK1-RIPK3-mixed lineage kinase domain-like protein (MLKL), which is complex II. RIPK3 phosphorylates MLKL, ultimately leading to necrosis through plasma membrane disruption and cell lysis. Current studies suggest that necroptosis is associated with the pathogenesis of neuroinflammatory diseases, such as Alzheimer’s disease, Parkinson’s disease, and traumatic brain injury. Inhibitors of necroptosis, such as necrostatin-1 (Nec-1) and stable variant of Nec (Nec-1s), have been proven to be effective in many neurological diseases. The purpose of this article is to illuminate the mechanism underlying necroptosis and the important role that necroptosis plays in neuroinflammatory diseases. Overall, this article shows a potential therapeutic strategy in which targeting necroptotic factors may improve the pathological changes and clinical symptoms of neuroinflammatory disorders.

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Section: Necroptosismentioning

confidence: 99%

Necroptosis: A Novel Pathway in Neuroinflammation

Jiang

et al. 2021

Front. Pharmacol.

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“…Apoptosis, the form of programmed cell death, is elicited with extrinsic and intrinsic stimuli through caspases-mediated extrinsic and intrinsic death pathway [17]. Both the blockage of NF-κB signaling and induction of apoptosis have been indicated to participate in the inhibition of CRC progression by CHMs [10,18].…”

Section: Introductionmentioning

confidence: 99%

Suppression of PKCδ/NF-κB Signaling and Apoptosis Induction through Extrinsic/Intrinsic Pathways Are Associated with Magnolol-Inhibited Tumor Progression in Colorectal Cancer In Vitro and In Vivo

Kuan

Chen

et al. 2020

IJMS

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Magnolol is one of the hydroxylated biphenyl compounds from the root and stem bark of Magnolia officinalis, which shown to possess anti-colorectal cancer (CRC) effects. However, the regulatory mechanism of magnolol on apoptosis and NF-κB signaling in human CRC has not been elucidated. Thus, we investigated the inhibitory mechanism of magnolol on human and mouse CRC (HT-29 and CT-26) in vitro and in vivo. Results from reporter gene assay indicated that both magnolol and rottlerin (PKCδ inhibitor) reduced the endogenous NF-κB activity. In addition, indolactam V (PKCδ activator)-induced NF-κB signaling was significantly suppressed with both magnolol and rottlerin treatment. Results from Western blotting also indicated that phosphorylation of PKCδ and NF-κB -related proteins involved in tumor progression were effectively decreased by magnolol treatment. The invasion capacity of CRC cells was also attenuated by both magnolol and rottlerin. Furthermore, magnolol triggered Fas/Fas-L mediated extrinsic apoptosis and mitochondria mediated intrinsic apoptosis were validated by flow cytometry. Most importantly, tumor growth in both HT-29 and CT-26 bearing mice were suppressed by magnolol, but no pathologic change was detected in mice kidney, spleen, and liver. As confirmed by immunohistochemistry (IHC) staining from tumor tissue, PKCδ/NF-κB signaling and downstream proteins expression were decreased, while apoptotic proteins expression was increased in the magnolol treated group. According to these results, we suggest that the induction of apoptosis through extrinsic/intrinsic pathways and the blockage of PKCδ/NF-κB signaling are associated with the magnolol-inhibited progression of CRC.

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“…These cells normally express molecules called death ligands (DL) on their surfaces, which recognize target cells, either by ligation of the DLs to the death receptors (DRs) on the surface of these cells, or by secretion of cytolytic molecules (i.e. perforin and granzyme) [37]. Adaptor proteins cause initiator procaspases to cluster together leading to a conformational change that activates the procaspases.…”

Section: Extrinsic Phasementioning

confidence: 99%

“…The Tumor Necrosis Factor Receptor (TNFR) -associated death domain (TRADD) was found associated with TNF-R1 upon binding of TNFα. The DD-containing molecules are specialized adapter molecules coupling to the apoptosis executioners, which are in many instances members of the caspase family of proteases [37][38]. The best characterized member of these receptor-binding caspases is caspase-8.…”

Section: Extrinsic Phasementioning

confidence: 99%

Apoptosis, guardian of the genome: Review

Khalil¹

2021

World J. Bio. Pharm. Health Sci.

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Apoptosis has attracted great attention in the last two decades and the number of publications related to apoptosis has been growing exponentially. The revolution that has occurred in apoptosis research is a direct result of a better understanding of the genetic program and biochemical mechanisms of apoptosis. Apoptosis is not only a common normal event but also essential for the growth and development of organisms. In the adult, apoptosis is mostly abnormal, but in its absence or failure cancer cells obtain immortality by escaping this type of cell death. Apoptosis works synergistically in intrinsic and extrinsic pathways. The first pathway is initiated by the cell itself in response to stress. The second is initiated via death receptors stimulated by cells of the immune system. This review is an attempt to answer questions like: Why is cell death important to study? How cells undergo apoptosis? What controls the decision between life and death? Which cellular events could cause the control of apoptosis to be impaired? The literature cited below shows some sort of unity in the scientific community on the necessity of a sophisticated balance between “pro-survival” and “pro-death” forces to ensure the happiness of cells in multicellular organisms

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Destined to Die: Apoptosis and Pediatric Cancers

Cited by 14 publications

References 187 publications

Necroptosis: A Novel Pathway in Neuroinflammation

Necroptosis: A Novel Pathway in Neuroinflammation

Suppression of PKCδ/NF-κB Signaling and Apoptosis Induction through Extrinsic/Intrinsic Pathways Are Associated with Magnolol-Inhibited Tumor Progression in Colorectal Cancer In Vitro and In Vivo

Apoptosis, guardian of the genome: Review

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