scholarly journals Metabolomics analysis reveals aminoquinazolin derivative 9d-induced oxidative stress and cell cycle arrest in A549 cells

RSC Advances ◽  
2017 ◽  
Vol 7 (22) ◽  
pp. 13149-13158 ◽  
Author(s):  
Wenrui Liu ◽  
Feng Jin ◽  
Dan Gao ◽  
Lu Song ◽  
Chao Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
A549 Cells ◽  
Cycle Arrest ◽  
A549 Lung ◽  
Metabolomics Analysis ◽  
Tof Ms

An UPLC/Q-TOF MS based metabolomics approach was established to study the probable antitumor mechanism of aminoquinazolin derivative 9d, which could induce oxidative stress and cell cycle arrest in A549 lung cancer cells.

scholarly journals Middle Infrared Radiation Induces G2/M Cell Cycle Arrest in A549 Lung Cancer Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54117 ◽  
Author(s):  
Hsin-Yi Chang ◽  
Meng-Her Shih ◽  
Hsuan-Cheng Huang ◽  
Shang-Ru Tsai ◽  
Hsueh-Fen Juan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Infrared Radiation ◽  
Lung Cancer Cells ◽  
M Cell ◽  
Cycle Arrest ◽  
Middle Infrared ◽  
A549 Lung

scholarly journals 18β-Glycyrrhetinic Acid Has Anti-Cancer Effects via Inducing Apoptosis and G2/M Cell Cycle Arrest, and Inhibiting Migration of A549 Lung Cancer Cells

2021 ◽  
Vol Volume 14 ◽  
pp. 5131-5144
Author(s):  
Ying-Hua Luo ◽  
Cheng Wang ◽  
Wan-Ting Xu ◽  
Yu Zhang ◽  
Tong Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Glycyrrhetinic Acid ◽  
Lung Cancer Cells ◽  
M Cell ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
A549 Lung

Arsenic trioxide inhibits the growth of human lung cancer cell lines via cell cycle arrest and induction of apoptosis at both normoxia and hypoxia

2009 ◽  
Vol 25 (8) ◽  
pp. 505-515 ◽  
Author(s):  
Qu Ge-ping ◽  
Xiu Qing-Yu ◽  
Li Bing ◽  
Liu Yong-an ◽  
Zhang Ling-Zhen
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Lung ◽  
A549 Cells ◽  
Cyclin B ◽  
M Cell ◽  
Cycle Arrest ◽  
Induction Of Apoptosis

Arsenic trioxide (As 2O3) has been established to be an effective agent for treating acute promyleocytic leukemia. Laboratory data suggest that As2O 3 induces apoptosis of several solid tumor cells including lung cancer cells. Regions of tissue hypoxia often arise in aggressive solid tumors, and hypoxic tumors exhibit augmented invasiveness and metastatic ability in several malignancies. Furthermore, hypoxia may impair the treatment efficiency; therefore, we studied the cytotoxic effect of As2O3 on human lung adenocarcinoma cell lines A549 and A549/R (resistant to vincristine, adriamycin and mitomycin etc.) grown under normoxic and hypoxic (1% oxygen) conditions. At both normoxia and hypoxia, 5, 10 and 15 µM As2O3 induced evident growth inhibition and apoptosis in A549 cells as well as A549/R cells after 48 hours of exposure. In contrast, the conventional chemotherapeutic drug vincristine showed lowered efficiency in hypoxic A549 cells. As2O3 induced G2/M cell cycle arrest in both normoxic and hypoxic A549 cells. As2O3 significantly decreased the messenger RNA (mRNA) levels of Cyclin B1 and survivin and the protein levels of Cyclin B1, phospho-CDC2 (Thr 161) and survivin in both normoxic and hypoxic A549 cells. Together, our findings indicated that As2O3 significantly inhibited the proliferation of lung cancer cells via G2/M cell cycle arrest and induction of apoptosis at both normoxia and hypoxia, and the induction of apoptosis was associated with down regulation of survivin.

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