scholarly journals Combination treatment with arsenic trioxide and sulindac enhances apoptotic cell death in lung cancer cells via activation of oxidative stress and mitogen-activated protein kinases

1994 ◽  
Author(s):  
Hak-Ryul Kim
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Protein Kinases ◽  
Combination Treatment ◽  
Apoptotic Cell ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

scholarly journals Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

Molecules ◽  
2019 ◽  
Vol 25 (1) ◽  
pp. 144 ◽  
Author(s):  
Chang-Hyun Park ◽  
Ji Hoon Song ◽  
Su-Nam Kim ◽  
Ji Hwan Lee ◽  
Hae-Jeung Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Protein Kinases ◽  
Apoptotic Cell ◽  
Curcuma Longa ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ht22 Cells ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

In the central nervous system, glutamate is a major excitable neurotransmitter responsible for many cellular functions. However, excessive levels of glutamate induce neuronal cell death via oxidative stress during acute brain injuries as well as chronic neurodegenerative diseases. The present study was conducted to examine the effect of tetrahydrocurcumin (THC), a major secondary metabolite of curcumin, and its possible mechanism against glutamate-induced cell death. We prepared THC using curcumin isolated from Curcuma longa (turmeric) and demonstrated the protective effect of THC against glutamate-induced oxidative stress in HT22 cells. THC abrogated glutamate-induced HT22 cell death and showed a strong antioxidant effect. THC also significantly reduced intracellular calcium ion increased by glutamate. Additionally, THC significantly reduced the accumulation of intracellular oxidative stress induced by glutamate. Furthermore, THC significantly diminished apoptotic cell death indicated by annexin V-positive in HT22 cells. Western blot analysis indicated that the phosphorylation of mitogen-activated protein kinases including c-Jun N-terminal kinase, extracellular signal-related kinases 1/2, and p38 by glutamate was significantly diminished by treatment with THC. In conclusion, THC is a potent neuroprotectant against glutamate-induced neuronal cell death by inhibiting the accumulation of oxidative stress and phosphorylation of mitogen-activated protein kinases.

scholarly journals Combination treatment with arsenic trioxide and phytosphingosine enhances apoptotic cell death in arsenic trioxide–resistant cancer cells

2007 ◽  
Vol 6 (1) ◽  
pp. 82-92 ◽  
Author(s):  
Moon-Taek Park ◽  
Young-Hee Kang ◽  
In-Chul Park ◽  
Chun-Ho Kim ◽  
Yun-Sil Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Combination Treatment ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Inhibition of mitogen activated protein kinases increases the sensitivity of A549 lung cancer cells to the cytotoxicity induced by a kava chalcone analog

2012 ◽  
Vol 424 (3) ◽  
pp. 488-492 ◽  
Author(s):  
Janel K. Warmka ◽  
Eric L. Solberg ◽  
Nicholette A. Zeliadt ◽  
Balasubramanian Srinivasan ◽  
Aaron T. Charlson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Protein Kinases ◽  
Lung Cancer Cells ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
A549 Lung

MicroRNA (miR)-355 Suppressed Small Cell Lung Cancer Cell Metastasis via Regulating P38 Mitogen-Activated Protein Kinases (MAPKs) Signaling

2021 ◽  
Vol 11 (11) ◽  
pp. 2197-2202
Author(s):  
Peng Wang ◽  
Chong Bai ◽  
Zhenli Hu ◽  
Xingjing Li ◽  
Fang Shen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinases ◽  
Small Cell ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Blank Group ◽  
Mitogen Activated Protein Kinases ◽  
Cell Metastasis ◽  
Mitogen Activated Protein ◽  
P38 Mapks

MicroRNA (miR)-355 was reported to mediate p38 mitogen-activated protein kinases (MAPKs) signaling, which exerted an effect on cell invasion and metastasis. But whether miR-355 could inhibit small cell lung cancer cell line H446 cell metastasis by regulating p38 MAPKs signaling needs further study. H446 cells were cultured to establish miR-355 overexpression group and blank group. The expression of MT1-MMP, the activity and migration of H446 cells were evaluated. Further, the ability of invasion, the level of p-p38 MAPKs and the activity degree of MT1-MMP were observed in H446 cells. MT1-MMP was mainly expressed on the cell membrane. miR-355 overexpression significantly decreased cellular viability and reduced MT1-MMP and p-p38 MAPKs levels relative to the blank group without influencing p38 MAPKs level. In addition, miR-355 overexpression suppressed cell migration and invasive ability in H446 cells. Finally, miR-355 overexpression reduced pro-MMP and MMP-2 activity in H446 cells. miR-355 overexpression suppressed H446 cell metastasis through regulating P38 MAPKs signaling.

scholarly journals Myrcene Exhibits Antitumor Activity Against Lung Cancer Cells by Inducing Oxidative Stress and Apoptosis Mechanisms

2020 ◽  
Vol 15 (9) ◽  
pp. 1934578X2096118
Author(s):  
Xudong Bai ◽  
Jin Tang
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Metabolic Activity ◽  
Lung Cancer Cells ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
A549 Lung

Myrcene, a natural olefinic hydrocarbon, possesses anti-inflammatory, analgesic, antibiotic, and antimutagenic properties, but its anticancer effect has not yet been elucidated. Hence, the present study was framed to investigate the molecular mechanism by which myrcene mediates the anticancer activity of A549 lung adenocarcinoma cells. In vitro, A549 lung cancer cells were cultured either with or without myrcene, and the effects on cellular metabolic activity, levels of reactive oxygen species (ROS), mitochondrial integrity, deoxyribonucleic acid (DNA) damage, and activity of caspases were analyzed. The study demonstrated that compared with control cells, myrcene induces cell death in a dose-dependent manner while inducing ROS levels. Further experiments revealed that the metabolic activity of the A549 lung adenocarcinoma cells was diminished with increased DNA damage and altered cellular integrity. In addition, increased activity of caspase-3 was also evidenced with reduced mitochondrial membrane potential synthesis in the myrcene-treated cells, which demonstrate that lung cancer cells experience signs of toxicity during myrcene treatment through the activation of the apoptosis mechanism via mitochondria-mediated cell death signaling and induction of oxidative stress. The results provide the first report on the evidence of anticancer activity and the possibility of a new drug that could be used for the treatment of lung cancer.

scholarly journals Increased Oxidative Stress Induced by Rubus Bioactive Compounds Induce Apoptotic Cell Death in Human Breast Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Blassan P. George ◽  
Heidi Abrahamse
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cell Death ◽  
Cytochrome C ◽  
Cancer Cells ◽  
Bioactive Compounds ◽  
Breast Cancer Cells ◽  
Apoptotic Cell ◽  
Ros Production ◽  
Caspase 9

Bioactive compounds from plants represent good candidate drugs for the prevention and treatment of various forms of cancer. Berries are rich sources of bioactive compounds, and there has been an increasing interest in the study of therapeutic action of wild berries. Oxidants are generated continuously in biological system as a result of physiological process. When there is an imbalance between oxidants and antioxidants, it leads to a condition called oxidative stress. Natural compounds as inducers of oxidative stress are able to modulate the physiological functions of cancer cells leading to cell death or survival. The aim of this study was to evaluate the induction of apoptosis by isolated bioactive compounds (1-(2-hydroxyphenyl)-4-methylpentan-1-one (C1) and 2-[(3-methylbutoxy) carbonyl] benzoic acid (C2)) from Rubus fairholmianus against MCF-7 breast cancer cells. The exposure of C1 and C2 reduced viability (IC50 of C1: 4.69; C2: 8.36 μg/mL) and proliferation. Cytochrome c release from mitochondria and changes in mitochondrial membrane potential of treated cells supported the intrinsic apoptotic cell death. Reactive oxygen species (ROS) production after treatment with C1 and C2 was found to be higher and induced nuclear damage. Expression of apoptotic proteins after the treatments was significantly upregulated as indicated using immunofluorescence (caspase 9, p53, and Bax), western blotting (p53, cleaved PARP, cytochrome c, and Bax), and ELISA (caspase 9) analysis. Overall, C1 was more cytotoxic, increased the ROS production in dichlorodihydrofluorescein diacetate assay, and induced apoptosis in breast cancer cells. These results illustrate that berry bioactive compounds have strong chemopreventive potential. In this article, we provide information on prooxidant and anticancer activities of Rubus bioactive compounds. Natural products have always demonstrated a significant contribution to the development of several cancer chemotherapeutic drugs. Most of these compounds are known to affect the redox state of the cell; and studies on these compounds have focused on their antioxidant property instead of prooxidant properties.

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