• Archives of Pharmacal Research
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• v.19 no.2
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• pp.91-94
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• 1996

In the course of a search for antitumor agents, we found that the extract of Curcuma longa was effective in inducing apoptosis or programmed cell death (PCD) in human myeloid leukemia cells (HL-60). Active compounds for PCD were isolated from the hexanic extraction of the rhizome of Curcuma longa. With the several chromatographies, and spectral data, they were identified as ar-turmerone and $\beta-atlantone$. The present results demonstrate that the exposure of human myeloid leukemia HL-60 cells to clinically achievable concentrations of arturmerone (TU) or .$\beta-atlantone$(AT) produced internucleosomal DNA fragmentation of approximately 200 base-pair multiples, and the morphological changes characteristic of cells undergoing apoptosis or PCD. This findings suggest that these agents may exert their antitumoral activity, in part, through induction of apoptosis(PCD).

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.145-145
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• 2003

Familial form of Alzheimer's disease (FAD) is caused by mutations in presenilin-1 (PS-1) and presenilin-2 (PS-2). PS1 and PS2 mutation are known to similar effects on the production of amyloid ${\beta}$ peptide (A${\beta}$) and cause of neuronal cell death in the brain of patient of AD. The importance of the alternation of cellular calcium homeostasis in the neuronal cell death by PS1 mutation in a variety of experimental systems has been demonstrated.(omitted)

• Toxicological Research
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• v.26 no.2
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• pp.109-115
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• 2010

The purpose of this study was to elucidate the mechanism underlying enhanced radiosensitivity to $^{60}Co\;{\gamma}$-irradiation in human prostate PC-3 cells pretreated with berberine. The cytotoxic effect of the combination of berberine and irradiation was superior to that of berberine or irradiation alone. Cell death and Apoptosis increased significantly with the combination of berberine and irradiation. Additionally, ROS generation was elevated by berberine with or without irradiation. The antioxidant NAC inhibited berberine and radiation-induced cell death. Bax, caspase-3, p53, p38, and JNK activation increased, but activation of Bcl-2, ERK, and HO-1 decreased with berberine treatment with or without irradiation. Berberine inhibited the anti-apoptotic signal pathway involving the activation of the HO-1/NF-${\kappa}B$-mediated survival pathway, which prevents radiation-induced cell death. Our data demonstrate that berberine inhibited the radioresistant effects and enhanced the radiosensitivity effects in human prostate cancer cells via the MAPK/caspase-3 and ROS pathways.

• Molecules and Cells
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• v.39 no.1
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• pp.72-76
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• 2016

Cell death pathways such as apoptosis can be activated in response to oxidative stress, enabling the disposal of damaged cells. In contrast, controlled intracellular redox events are proposed to be a significant event during apoptosis signaling, regardless of the initiating stimulus. In this scenario oxidants act as second messengers, mediating the post-translational modification of specific regulatory proteins. The exact mechanism of this signaling is unclear, but increased understanding offers the potential to promote or inhibit apoptosis through modulating the redox environment of cells. Peroxiredoxins are thiol peroxidases that remove hydroperoxides, and are also emerging as important players in cellular redox signaling. This review discusses the potential role of peroxiredoxins in the regulation of apoptosis, and also their ability to act as biomarkers of redox changes during the initiation and progression of cell death.

• Biomolecules & Therapeutics
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• v.27 no.2
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• pp.145-151
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• 2019

Methamphetamine (METH) acts strongly on the nervous system and damages neurons and is known to cause neurodegenerative diseases such as Alzheimer's and Parkinson's. Flavonoids, polyphenolic compounds present in green tea, red wine and several fruits exhibit antioxidant properties that protect neurons from oxidative damage and promote neuronal survival. Especially, epicatechin (EC) is a powerful flavonoid with antibacterial, antiviral, antitumor and antimutagenic effects as well as antioxidant effects. We therefore investigated whether EC could prevent METH-induced neurotoxicity using HT22 hippocampal neuronal cells. EC reduced METH-induced cell death of HT22 cells. In addition, we observed that EC abrogated the activation of ERK, p38 and inhibited the expression of CHOP and DR4. EC also reduced METH-induced ROS accumulation and MMP. These results suggest that EC may protect HT22 hippocampal neurons against METH-induced cell death by reducing ER stress and mitochondrial damage.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.143.1-143.1
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• 2003

In this study. we investigated whether the cardioprotective effect shown by quercetin 3-O-$\alpha$-arabinofuranoside extracted from Lindera erythrocarpa against ROS-induced cell death in H9c2 cardiac myocytes. Cell death was induced by BSO, buthionine sulfoximine, which inhibits GSH level and subsequntly increase ROS level. Cell death was quntitatively determined by measuring lactate dehydrogenase (LDH) activity. (omitted)

• BMB Reports
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• v.56 no.3
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• pp.145-152
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• 2023

Mechanosensitive ion channels sense mechanical stimuli applied directly to the cellular membranes or indirectly through their tethered components, provoking cellular mechanoresponses. Among others, Piezo1 mechanosensitive ion channel is a relatively novel Ca²⁺-permeable channel that is primarily present in non-sensory tissues. Recent studies have demonstrated that Piezo1 plays an important role in Ca²⁺-dependent cell death, including apoptosis and ferroptosis, in the presence of mechanical stimuli. It has also been proven that cancer cells are sensitive to mechanical stresses due to higher expression levels of Piezo1 compared to normal cells. In this review, we discuss Piezo1-mediated cell death mechanisms and therapeutic strategies to inhibit or induce cell death by modulating the activity of Piezo1 with pharmacological drugs or mechanical perturbations induced by stretch and ultrasound.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.6
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• pp.2251-2256
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• 2015

To study effects of cellular FLICE (FADD-like IL-$1{\beta}$-converting enzyme)-inhibitory protein (c-FLIP) inhibition by RNA interference (RNAi) on sensitivity of U2OS cells to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, plasmid pSUPER-c-FLIP-siRNA was constructed and then transfected into U2OS cells. A stable transfection cell clone U2OS/pSUPER-c-FLIP-siRNA was screened from the c-FLIP-siRNA transfected cells. RT-PCR and Western blotting were applied to measure the expression of c-FLIP at the levels of mRNA and protein. The results indicated that the expression of c-FLIP was significantly suppressed by the c-FLIP-siRNA in the cloned U2OS/pSUPER-c-FLIP-siRNA as compared with the control cells of U2OS/pSUPER. The cloned cell line of U2OS/pSUPER-c-FLIP-siRNA was further examined for TRAILinduced cell death and apoptosis in the presence of a pan-antagonist of inhibitor of apoptosis proteins (IAPs) AT406, with or without 4 hrs pretreatment with rocaglamide, an inhibitor of c-FLIP biosynthesis, for 24 hrs. Cell death effects and apoptosis were measured by the methods of MTT assay with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry, respectively. The results indicated that TRAIL-induced cell death in U2OS/pSUPER-c-FLIP-siRNA was increased compared with control cells U2OS/pSUPER in the presence or absence of AT406. Flow cytometry indicated that TRAIL-induced cell death effects proceeded through cell apoptosis pathway. However, in the presence of rocaglamide, cell death or apoptotic effects of TRAIL were similar and profound in both cell lines, suggesting that the mechanism of action for both c-FLIP-siRNA and rocaglamide was identical. We conclude that the inhibition of c-FLIP by either c-FLIP-siRNA or rocaglamide can enhance the sensitivity of U2OS to TRAIL-induced apopotosis, suggesting that inhibition of c-FLIP is a good target for anti-cancer therapy.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.1
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• pp.91-96
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• 2015

A lipopeptide extract of Bacillus amyloliquefaciens BACY1 (BLE) was found to induce cell death in human oral squamous cell carcinoma (OSCC) cell lines, SCC4 and SCC25, in this study. The results of MTT assay showed that BLE inhibited OSCC cell proliferation in a dose-dependent manner. BLE was also effective in increasing the sub-G1 phases. Furthermore, when membrane damage in SCC4 cells treated with BLE was monitored by LDH assay, release of LDH was significantly increased. The protein and mRNA levels of pro-apoptotic Bax, and caspase-3 were up-regulated by BLE. Taken together, these results suggest that BLE induces apoptosis and then inhibits the cell proliferation of human OSCC cells.

• International Journal of Contents
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• v.8 no.4
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• pp.74-77
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• 2012

Radiation has been an effective tool for treating cancer for a long time. Radiation therapy induces DNA damage within cancer cells and destroys their ability to reproduce. Radiation therapy is often combined with other treatments, like surgery and chemotherapy. Here, we describe the effects of radiation and histone deacetylase inhibitor, Trichostain A, on cell cycle regulation in hepatoma cells. The combinatorial treatment of radiation and Trichostain A induced cell cycle arrest and thereby increasing the hepatoma cell death. Furthermore, the regulatory effects of radiation and Trichostatin A on cell cycle applied in cell type specifically. These results suggest that the treatment of radiation and Trichostatin A may play a central role in hepatoma cell death and might be a good remedy to improve the efficiency of radiation therapy.