scholarly journals Apoptotic Effects of Anthocyanins from Vitis coignetiae Pulliat Are Enhanced by Augmented Enhancer of the Rudimentary Homolog (ERH) in Human Gastric Carcinoma MKN28 Cells

2021 ◽  
Vol 22 (6) ◽  
pp. 3030
Author(s):  
Cheol Park ◽  
Won Sup Lee ◽  
Se-Il Go ◽  
Sang-Ho Jeong ◽  
Jiyun Yoo ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Ros Generation ◽  
Human Gastric Cancer ◽  
Oxygen Species ◽  
Mitochondrial Depolarization ◽  
Gastric Cancer Cells ◽  
Anticancer Efficacy ◽  
Antiapoptotic Proteins ◽  
Apoptotic Effect ◽  
Apoptotic Effects

Evidence suggests that augmented expression of a certain gene can influence the efficacy of targeted and conventional chemotherapies. Here, we tested whether the high expression of enhancer of the rudimentary homolog (ERH), which serves as a prognostic factor in some cancers, can influence the efficacy of anthocyanins isolated from fruits of Vitis coignetiae Pulliat, Meoru in Korea (AIMs) on human gastric cancer cells. The anticancer efficacy of AIMs was augmented in ERH-transfected MKN28 cells (E-MKN28 cells). Molecularly, ERH augmented AIM-induced caspase-dependent apoptosis by activating caspase-3 and -9. The ERH-augmented apoptotic effect was related to mitochondrial depolarization and inhibition of antiapoptotic proteins, XIAP, and Bcl-2. In addition, reactive oxygen species (ROS) generation was augmented in AIMs-treated E-MKN28 cells compared to AIMs-treated naïve MKN28 cells. In conclusion, ERH augmented AIM-induced caspase-dependent mitochondrial-related apoptosis in MKN28 cells. A decrease in expression of Bcl-2 and subsequent excessive ROS generation would be the mechanism for ERH-augmented mitochondrial-related apoptosis in AIMs-treated MKN28 cells. A decrease in expression of XIAP would be another mechanism for ERH-augmented caspase-dependent apoptosis in AIMs-treated MKN28 cells.

scholarly journals Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3

2001 ◽  
Vol 93 (6) ◽  
pp. 916-916 ◽  
Author(s):  
XH Jiang ◽  
BCY Wong ◽  
ST Yuen ◽  
SH Jiang ◽  
CH Cho ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Caspase 3 ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals Agaricus blazeiExtract Induces Apoptosis through ROS-Dependent JNK Activation Involving the Mitochondrial Pathway and Suppression of Constitutive NF-κB in THP-1 Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Mun-Ock Kim ◽  
Dong-Oh Moon ◽  
Jin Myung Jung ◽  
Won Sup Lee ◽  
Yung Hyun Choi ◽  
...  
Keyword(s):  
Mitochondrial Pathway ◽  
Ros Generation ◽  
Gene Products ◽  
Oxygen Species ◽  
Agaricus Blazei ◽  
Anti Cancer ◽  
Induced Apoptosis ◽  
Jnk Activation ◽  
Apoptotic Effects ◽  
Apoptotic Mechanism

Agaricus blazeiis widely accepted as a traditional medicinal mushroom, and it has been known to exhibit immunostimulatory and anti-cancer activity. However, the apoptotic mechanism in cancer cells is poorly understood. In this study, we have investigated whetherA. blazeiextract (ABE) exerts antiproliferative and apoptotic effects in human leukemic THP-1 cells. We observed that ABE-induced apoptosis is associated with the mitochondrial pathway, which is mediated by reactive oxygen species (ROS) generation and prolonged c-Jun N-terminal kinase (JNK) activation. In addition, the ABE treatment resulted in the accumulation of cytochromecin the cytoplasm, an increase in caspase activity, and an upregulation of Bax and Bad. With those results in mind, we found that ABE decreases constitutive NF-κB activation and NF-κB-regulated gene products such as IAP-1 and -2. We concluded that ABE induces apoptosis with ROS-dependent JNK activation and constitutive activated NF-κB inhibition in THP-1 cells.

scholarly journals Apoptotic effects of hsian‐tsao ( Mesona procumbens Hemsley) on hepatic stellate cells mediated by reactive oxygen species and ERK, JNK, and caspase‐3 pathways

2019 ◽  
Vol 7 (5) ◽  
pp. 1891-1898
Author(s):  
Yung‐Hsiang Yeh ◽  
Chun‐Ya Liang ◽  
Mao‐Liang Chen ◽  
Fu‐Ming Tsai ◽  
Yi‐Ying Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hepatic Stellate Cells ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Stellate Cells ◽  
Oxygen Species ◽  
Apoptotic Effects

scholarly journals Blockade of Histone Deacetylase Inhibitor-Induced RelA/p65 Acetylation and NF-κB Activation Potentiates Apoptosis in Leukemia Cells through a Process Mediated by Oxidative Damage, XIAP Downregulation, and c-Jun N-Terminal Kinase 1 Activation

2005 ◽  
Vol 25 (13) ◽  
pp. 5429-5444 ◽  
Author(s):  
Yun Dai ◽  
Mohamed Rahmani ◽  
Paul Dent ◽  
Steven Grant
Keyword(s):  
Oxidative Damage ◽  
Nuclear Translocation ◽  
Hdac Inhibitors ◽  
Histone Acetyltransferases ◽  
Leukemia Cells ◽  
Ros Generation ◽  
Suberoylanilide Hydroxamic Acid ◽  
Oxygen Species ◽  
Antiapoptotic Proteins ◽  
Deacetylase Inhibitor

ABSTRACT NF-κB activation is reciprocally regulated by RelA/p65 acetylation and deacetylation, which are mediated by histone acetyltransferases (HATs) and deacetylases (HDACs). Here we demonstrate that in leukemia cells, NF-κB activation by the HDAC inhibitors (HDACIs) MS-275 and suberoylanilide hydroxamic acid was associated with hyperacetylation and nuclear translocation of RelA/p65. The latter events, as well as the association of RelA/p65 with IκBα, were strikingly diminished by either coadministration of the IκBα phosphorylation inhibitor Bay 11-7082 (Bay) or transfection with an IκBα superrepressor. Inhibition of NF-κB by pharmacological inhibitors or genetic strategies markedly potentiated apoptosis induced by HDACIs, and this was accompanied by enhanced reactive oxygen species (ROS) generation, downregulation of Mn-superoxide dismutase and XIAP, and c-Jun N-terminal kinase 1 (JNK1) activation. Conversely, N-acetyl l-cysteine blocked apoptosis induced by Bay/HDACIs by abrogating ROS generation. Inhibition of JNK1 activation attenuated Bay/HDACI lethality without affecting NF-κB inactivation and ROS generation. Finally, XIAP overexpression dramatically protected cells against the Bay/HDACI regimen but failed to prevent ROS production and JNK1 activation. Together, these data suggest that HDACIs promote the accumulation of acetylated RelA/p65 in the nucleus, leading to NF-κB activation. Moreover, interference with these events by either pharmacological or genetic means leads to a dramatic increase in HDACI-mediated lethality through enhanced oxidative damage, downregulation of NF-κB-dependent antiapoptotic proteins, and stress-related JNK1 activation.

Nitric oxide-dependent pro-oxidant and pro-apoptotic effect of metallothioneins in HL-60 cells challenged with cupric nitrilotriacetate

2001 ◽  
Vol 354 (2) ◽  
pp. 397-406 ◽  
Author(s):  
Shang-Xi LIU ◽  
Kazuaki KAWAI ◽  
Vladimir A. TYURIN ◽  
Yulia Y. TYURINA ◽  
Grigory G. BORISENKO ◽  
...  
Keyword(s):  
Dna Cleavage ◽  
Caspase 3 ◽  
Protective Role ◽  
Membrane Phospholipids ◽  
No Donor ◽  
Redox Active ◽  
Apoptotic Effect ◽  
Transition And Heavy Metals ◽  
Apoptotic Effects

Intracellular safeguarding functions of metallothioneins (MTs) include sequestering transition and heavy metals, scavenging free radicals and protecting against electrophiles. We report that MT protection against Cu-induced cytotoxicity can be reversed and pro-oxidant and pro-apoptotic effects can be induced in HL-60 cells exposed to NO. We demonstrate that in ZnCl2-pretreated HL-60 cells loaded with copper nitrilotriacetate (Cu-NTA), exposure to an NO donor, S-nitroso-N-acetyl penicillamine, resulted in S-nitrosylation and oxidation of MT cysteines. This disruption of MT Cu-binding thiolate clusters caused loosening and release of redox-active Cu, enhanced redox-cycling activity of Cu and increased peroxidation of major classes of membrane phospholipids. We also found that Cu-induced oxidative stress in ZnCl2-pretreated/Cu-NTA-loaded HL-60 cells was accompanied by apoptosis documented by characteristic changes of nuclear morphology, internucleosomal DNA cleavage, externalization of phosphatidylserine, release of cytochrome c from mitochondria into cytosol and activation of caspase-3. We conclude that in Cu-challenged cells, NO can reverse the protective role of MTs and convert them into pro-oxidant, pro-apoptotic implements.

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