scholarly journals Sulphureuine B, a drimane type sesquiterpenoid isolated from Laetiporus sulphureus induces apoptosis in glioma cells

2015 ◽  
Vol 10 (4) ◽  
pp. 844 ◽  
Author(s):  
Jing-Wei Zhang ◽  
Gong-Ling Wen ◽  
Lei Zhang ◽  
Dong-Mei Duan ◽  
Zhong-Hai Ren
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathways ◽  
Death Receptor ◽  
Glioma Cells ◽  
Edible Mushroom ◽  
Caspase 8 ◽  
Laetiporus Sulphureus ◽  
Death Receptor Signaling ◽  
Induced Apoptosis

<p class="Abstract">A drimane type sesquiterpenoids, sulphureuine B was isolated from the edible mushroom <em>Laetiporus sulphureus</em> and its antiproliferative properties were investigated using U-87MG glioma cells. It was observed that sulphu-reuine B-induced apoptosis in U-87MG cells and the mechanisms involved are endoplasmic reticulum stress, mitochondrial and death receptor mediated pathways. Endoplasmic reticulum stress was identified from the results of enormous cytoplasmic vacuolation, CHOP elevation and caspase-12 cleavage. Further, we found that treatment of sulphureuine B-induced PERK, IRE1α, and ATF6α activations. In addition, sulphureuine B-induced Bcl-2 down-regulation, cleavage of PARP, and caspase-8 activation were also affected. All these experimental results clearly revealed that sulphureuine B-induced apoptosis mediated through endoplasmic reticulum stress, mitochondrial, and death receptor signaling pathways.</p><p> </p>

scholarly journals Role of the Death Receptor and Endoplasmic Reticulum Stress Signaling Pathways in Polyphyllin I-Regulated Apoptosis of Human Hepatocellular Carcinoma HepG2 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Qihui Luo ◽  
Dandan Yang ◽  
Qi Qi ◽  
Chao Huang ◽  
Bing Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Signaling Pathways ◽  
Hepg2 Cells ◽  
Death Receptor ◽  
Receptor Signaling ◽  
Death Receptor Signaling

Polyphyllin has been reported to exhibit anticancer effects against various types of cancer via the proapoptotic signaling pathway. The aim of the present study was to investigate the role of the endoplasmic reticulum stress and death receptor signaling pathways in PPI-induced apoptosis of human hepatocellular carcinoma HepG2 cells. Analysis demonstrated that PPI could significantly inhibit the proliferation and induce apoptosis of HepG2 cells in a dose- and time-dependent manner. Investigation into the molecular mechanism of PPI indicated that PPI notably mediated ER stress activation via IRE-1 overexpression and activation of the caspase-12 to protect HepG2 cells against apoptosis. In addition, PPI markedly induced the expression of death receptors signaling pathways-associated factors, including tumor necrosis factor (TNF) receptor 1/TNF-αand FAS/FASL. Additionally, suppression of the death receptor signaling pathways with a caspase-8 inhibitor, Z-IETD-FMK, revealed an increase in the death rate and apoptotic rate of HepG2 cells. Collectively, the findings of the present study suggested that the ER stress and death receptor signaling pathways were associated with PPI-induced HepG2 cell apoptosis; however, endoplasmic reticulum stress may serve a protective role in this process. The combination of PPI and Z-IETD-FMK may activate necroptosis, which enhances apoptosis. Therefore, the results of the present study may improve understanding regarding the roles of signaling pathways in PPI regulated apoptosis and contribute to the development of novel therapies for the treatment of HCC.

scholarly journals The Chondroprotective Role of TMF in PGE2-Induced Apoptosis Associating with Endoplasmic Reticulum Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jianqiong Yang ◽  
Haiqing Liu ◽  
Linfu Li ◽  
Hai Liu ◽  
Weimei Shi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathways ◽  
Inflammatory Cytokine ◽  
Critical Role ◽  
Osteoarthritic Chondrocytes ◽  
Induced Apoptosis

Endoplasmic reticulum stress (ERS) has been demonstrated to exhibit a critical role in osteoarthritic chondrocytes. Whether 5,7,3′,4′-tetramethoxyflavone (TMF) plays the chondroprotective role in inhibition of PGE2-induced chondrocytes apoptosis associating with ERS has not been reported. To investigate this, the activation of PERK, ATF6, and IRE1 signaling pathways in ERS in chondrocytes pretreated with PGE2was studied. By treatment with PGE2, the chondrocytes apoptosis was significantly increased, the proapoptotic CHOP and JNK were upregulated, the prosurvival GRP78 and XBP1 were downregulated, and GSK-3βwas also upregulated. However, TMF exhibited the effectively protective functions via counteracting these detrimental effects of PGE2. Finally, the inflammatory cytokine PGE2can activate ERS signaling and promote chondrocytes apoptosis, which might be associated with upregulation of GSK-3β. TMF exhibits a chondroprotective role in inhibiting PGE2-induced ERS and GSK-3β.

scholarly journals The dual regulation of apoptosis by Flavivirus

2020 ◽  
Author(s):  
Yuhong Pan ◽  
Anchun Cheng ◽  
Mingshu Wang ◽  
Zhong Yin ◽  
Ren-Yong Jia
Keyword(s):  
Immune Response ◽  
Endoplasmic Reticulum ◽  
Signaling Pathways ◽  
Death Receptor ◽  
Scientific Basis ◽  
Research Progress ◽  
Host Defenses ◽  
Host Proteins ◽  
Infected Cells ◽  
Induced Apoptosis

Apoptosis is a form of programmed cell death, which maintains cellular homeostasis by eliminating pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria-mediated pathway and endoplasmic reticulum pathway. Its importance in host defenses is highlighted by the observation that many viruses evade, hinder or destroy apoptosis, thereby weakening the host’s immune response. Flaviviruses such as Dengue virus, Japanese encephalitis virus and West Nile virus utilize various strategies to activate or inhibit cell apoptosis. This article reviews the research progress of apoptosis mechanism during flaviviruses infection, including flaviviruses proteins to regulate apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses-induced apoptosis, which provides a scientific basis for understanding the pathogenesis of flaviviruses and helps in developing an effective antiviral therapy.

scholarly journals Anticancer Drugs Induce Caspase-8/FLICE Activation and Apoptosis in the Absence of CD95 Receptor/Ligand Interaction

Blood ◽  
1999 ◽  
Vol 93 (9) ◽  
pp. 3053-3063 ◽  
Author(s):  
Sebastian Wesselborg ◽  
Ingo H. Engels ◽  
Evi Rossmann ◽  
Marek Los ◽  
Klaus Schulze-Osthoff
Keyword(s):  
Anticancer Drugs ◽  
De Novo ◽  
Death Receptor ◽  
Dominant Negative ◽  
Caspase 8 ◽  
Drug Induced ◽  
Ligand Interaction ◽  
Caspase Family ◽  
Death Receptor Signaling ◽  
Induced Apoptosis

Abstract Proteases of the caspase family are the critical executioners of apoptosis. Their activation has been mainly studied upon triggering of death receptors, such as CD95 (Fas/APO-1) and tumor necrosis factor-R1, which recruit caspase-8/FLICE as the most proximal effector to the receptor complex. Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C. In Jurkat leukemic T cells, all drugs induced apoptosis and the cleavage of procaspase-8 to its active p18 subunit. However, cells resistant to CD95 were equally susceptible to anticancer drugs and activated caspase-8 with a similar kinetic and dose response as CD95-sensitive cells. The broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone prevented apoptosis and caspase-8 activation in response to CD95 and drug treatment, whereas a neutralizing CD95 decoy as well as a dominant-negative FADD construct selectively abrogated CD95, but not drug-induced effects. A potent activation of caspase-8 was also induced by cycloheximide, indicating that it was independent of protein synthesis. Our data, therefore, show that (1) anticancer drug-induced apoptosis does not require de novo synthesis of death ligands or CD95 interaction, and (2) that caspase-8 can be activated in the absence of a death receptor signaling.

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