Persimmon Leaf Extract Inhibits the ATM Activity during DNA Damage Response Induced by Doxorubicin in A549 Lung Adenocarcinoma Cells

2011 ◽  
Vol 75 (4) ◽  
pp. 650-655 ◽  
Author(s):  
Kayoko KAWAKAMI ◽  
Hiroshi NISHIDA ◽  
Naoto TATEWAKI ◽  
Yuki NAKAJIMA ◽  
Tetsuya KONISHI ◽  
...  

2010 ◽  
Author(s):  
Kayoko Nakayama-Kawakami ◽  
Hiroshi Nishida ◽  
Naoto Tatewaki ◽  
Yuki Nakajima ◽  
Testuya Konishi ◽  
...  


Cell Cycle ◽  
2010 ◽  
Vol 9 (11) ◽  
pp. 2170-2176 ◽  
Author(s):  
Ellen D. Jorgensen ◽  
Hong Zhao ◽  
Frank Traganos ◽  
Anthony P. Albino ◽  
Zbigniew Darzynkiewicz


2017 ◽  
Vol 90 ◽  
pp. 677-685 ◽  
Author(s):  
Meiling Yu ◽  
Benquan Qi ◽  
Wu Xiaoxiang ◽  
Jian Xu ◽  
Xiaolin Liu


FEBS Journal ◽  
2008 ◽  
Vol 275 (22) ◽  
pp. 5725-5732 ◽  
Author(s):  
Qiuxia He ◽  
Bin Huang ◽  
Jing Zhao ◽  
Yun Zhang ◽  
Shangli Zhang ◽  
...  


FEBS Letters ◽  
1998 ◽  
Vol 437 (1-2) ◽  
pp. 61-64 ◽  
Author(s):  
Fulu Bai ◽  
Takayoshi Matsui ◽  
Naoko Ohtani-Fujita ◽  
Yoshizumi Matsukawa ◽  
Yi Ding ◽  
...  


2018 ◽  
Vol 45 (3) ◽  
pp. 917-934 ◽  
Author(s):  
Fangqiong Li ◽  
Dongxiao Zhao ◽  
Suwen Yang ◽  
Juan Wang ◽  
Qin Liu ◽  
...  

Background/Aims: Triptolide (TP) is a diterpenoid triepoxide extracted from the traditional Chinese medical herb Tripterygium wilfordii that exerts prominent broad-spectrum anticancer activity to repress proliferation and induce cancer cell apoptosis through various molecular pathways. We previously observed that TP inhibits the progression of A549 cells and pancreatic cancer cells (PNCA-1) in vitro. However, the complex molecular mechanism underlying the anticancer activity of TP is not well understood. Methods: To explore the molecular mechanisms by which TP induces lung cancer cell apoptosis, we investigated changes in the protein profile of A549 cells treated with TP using a proteomics approach (iTRAQ [isobaric tags for relative and absolute quantitation] combined with NanoLC-MS/MS [nano liquid chromatography-mass spectrometry]). Changes in the profiles of the expressed proteins were analyzed using the bioinformatics tools OmicsBean and the Kyoto Encyclopedia of Genes and Genomes (KEGG) and were verified using western blotting. Apoptosis and cell cycle effects were analyzed using flow cytometry. Results: TP induced apoptosis in A549 cells and blocked A549 cells at the G2/M phase. Using iTRAQ technology, we observed 312 differentially expressed proteins associated in networks and implicated in different KEGG pathways. Gene Ontology (GO) analysis showed the overviews of dysregulated proteins in the biological process (BP), cell component (CC), and molecular function (MF) categories. Moreover, some candidate proteins involved in PARP1/AIF and nuclear Akt signaling pathways or metastasis processes were validated by western blotting. Conclusion: TP exerted anti-tumor activity on non-small cell lung cancer (NSCLC) A549 lung adenocarcinoma cells by dysregulating tumor-related protein expression. Herein, we provide a preliminary study of TP-related cytotoxicity on A549 cells using proteomics tools. These findings may improve the current understanding of the anti-tumor effects of TP on lung cancer cells and may reveal candidate proteins as potential targets for the treatment of lung cancer.



2020 ◽  
Vol 15 (9) ◽  
pp. 1934578X2096118
Author(s):  
Xudong Bai ◽  
Jin Tang

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.



2007 ◽  
Vol 60 (3) ◽  
pp. 449-457 ◽  
Author(s):  
Hiromi Sato ◽  
Keiko Fukumoto ◽  
Sachio Hada ◽  
Hiromi Hagiwara ◽  
Eriko Fujimoto ◽  
...  


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