Distinct CPT-induced deaths in lung cancer cells caused by clathrin-mediated internalization of CP micelles

Nanoscale ◽  
2016 ◽  
Vol 8 (6) ◽  
pp. 3510-3522 ◽  
Author(s):  
Yu-Sheng Liu ◽  
Ru-You Cheng ◽  
Yu-Lun Lo ◽  
Chin Hsu ◽  
Su-Hwei Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Chondroitin Sulfate ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Tumor Targeting ◽  
Therapeutic Outcome ◽  
Lung Cancer Cells ◽  
Cycle Arrest ◽  
Targeting Delivery

A chondroitin sulfate-graft-poly(ε-caprolactone), CP, was synthesized to encapsulate camptothecin (micelle/CPT) for tumor-targeting delivery. The therapeutic outcome of the micelle/CPT depends on internalization pathways and cell cycle arrest.

scholarly journals Overexpression of cyclin L2 induces apoptosis and cell-cycle arrest in human lung cancer cells

2007 ◽  
Vol 120 (10) ◽  
pp. 905-909 ◽  
Author(s):  
Hong-li LI ◽  
Tong-shan WANG ◽  
Xiao-yu LI ◽  
Nan LI ◽  
Ding-zhi HUANG ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Cycle Arrest ◽  
Human Lung Cancer Cells

Viriditoxin Induces G2/M Cell Cycle Arrest and Apoptosis in A549 Human Lung Cancer Cells

2015 ◽  
Vol 21 (4) ◽  
pp. 282 ◽  
Author(s):  
Ju Hee Park ◽  
Tae Hwan Noh ◽  
Haibo Wang ◽  
Nam Deuk Kim ◽  
Jee H. Jung
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
M Cell ◽  
Cycle Arrest ◽  
Human Lung Cancer Cells

Pycnidione, a fungus-derived agent, induces cell cycle arrest and apoptosis in A549 human lung cancer cells

2012 ◽  
Vol 197 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Che-Jen Hsiao ◽  
Shih-Hsin Hsiao ◽  
Wei-Lin Chen ◽  
Jih-Hwa Guh ◽  
George Hsiao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Cycle Arrest ◽  
Human Lung Cancer Cells

scholarly journals Albanol B from Mulberries Exerts Anti-Cancer Effect through Mitochondria ROS Production in Lung Cancer Cells and Suppresses In Vivo Tumor Growth

2020 ◽  
Vol 21 (24) ◽  
pp. 9502
Author(s):  
Thanh Nam Phan ◽  
Okwha Kim ◽  
Manh Tuan Ha ◽  
Cheol Hwangbo ◽  
Byung-Sun Min ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cyclin B1 ◽  
Lung Cancer Cells ◽  
Ros Production ◽  
Cycle Arrest ◽  
Mitochondrial Ros ◽  
Anti Cancer

Albanol B (ABN-B), an arylbenzofuran derivative isolated from mulberries, has been shown to have anti-Alzheimer’s disease, anti-bacterial and antioxidant activities. The aim of this study was to investigate the anti-cancer effect of this compound against lung cancer cells. The results show that ABN-B inhibited the proliferation of four human lung cancer cell lines (A549, BZR, H1975, and H226) and induced apoptosis, based on the cleavage of caspase-7 and PARP (poly (ADP-ribose) polymerase), as well as the downregulation of Bcl-2. ABN-B also induced cell cycle arrest at G2/M by down-regulating the expression of CKD1 (cyclin-dependent kinase 1) and cyclin B1, but up-regulating p21 (cyclin-dependent kinase inhibitor 1) expression. Notably, ABN-B increased the production of mitochondrial reactive oxygen species (ROS); however, treatment with mito-TEMPO (a specific mitochondrial antioxidant) blocked ABN-B-induced cell cycle arrest at G2/M and apoptosis, as well as the up-regulation of p21 and down-regulation of CDK1 and cyclin B1 induced by ABN-B. At the molecular level, ABN-B-induced mitochondrial ROS production increased the phosphorylation levels of AKT (protein kinase B) and ERK1/2 (extracellular signal-regulated kinase 1/2), while the inhibition of these kinases blocked the ABN-B-induced up-regulation of p21 and down-regulation of CDK1 and cyclin B1. Moreover, ABN-B significantly suppressed tumor growth in Ex-3LL (Lewis lung carcinoma) tumor-bearing mice. Taken together, these results suggest that ABN-B can exert an anti-cancer effect by inducing apoptosis and cell cycle arrest at G2/M through mitochondrial ROS production in lung cancer cells.

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