Regulation of the G1/S phase of the cell cycle and alterations in the RB pathway in human lung cancer

2006 ◽  
Vol 6 (4) ◽  
pp. 515-530 ◽  
Author(s):  
Harriet Wikman ◽  
Eeva Kettunen
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Human Lung ◽  
S Phase ◽  
Human Lung Cancer ◽  
Rb Pathway

scholarly journals Expression of G Protein-Coupled Receptor 19 in Human Lung Cancer Cells Is Triggered by Entry into S-Phase and Supports G2–M Cell-Cycle Progression

2012 ◽  
Vol 10 (10) ◽  
pp. 1343-1358 ◽  
Author(s):  
Stefan Kastner ◽  
Tilman Voss ◽  
Simon Keuerleber ◽  
Christina Glöckel ◽  
Michael Freissmuth ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Human Lung ◽  
S Phase ◽  
Human Lung Cancer ◽  
M Cell ◽  
Cycle Progression ◽  
Human Lung Cancer Cells ◽  
G Protein Coupled

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

scholarly journals Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid inhibits growth of human lung cancer A549 cells by arresting cell cycle and triggering apoptosis

2012 ◽  
Vol 24 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Li Li ◽  
George G. Chen ◽  
Ying-nian Lu ◽  
Yi Liu ◽  
Ke-feng Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer

scholarly journals 10-HDA Induces ROS-Mediated Apoptosis in A549 Human Lung Cancer Cells by Regulating the MAPK, STAT3, NF-κB, and TGF-β1 Signaling Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Xin-Mei Lin ◽  
Shao-Bin Liu ◽  
Ying-Hua Luo ◽  
Wan-Ting Xu ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Cycle Arrest ◽  
Human Lung Cancer Cells ◽  
Tgf Β1

10-Hydroxy-2-decenoic acid (10-HDA), also known as royal jelly acid, has a variety of physiological functions, and recent studies have shown that it also has anticancer effects. However, its anticancer mechanisms have not been clearly defined. In this study, we investigated the underlying mechanisms of 10-HDA in A549 human lung cancer cells. We used Cell Counting Kit-8 assay, scratch wound healing assay, flow cytometry, and western blot analysis to investigate its apoptotic effects and underlying mechanism. Our results showed that 10-HDA inhibited the proliferation of three types of human lung cancer cells and had no significant toxic effects on normal cells. Accompanying reactive oxygen species (ROS), 10-HDA induced A549 cell apoptosis by regulating mitochondrial-associated apoptosis, and caused cell cycle arrest at the G0/G1 phase in a time-dependent manner. Meanwhile, 10-HDA also regulated mitogen-activated protein kinase (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa B (NF-κB) signaling pathways by increasing the expression levels of phosphorylated c-Jun N-terminal kinase, p-p38, and I-κB, and additionally, by decreasing the expression levels of phosphorylated extracellular signal-regulated kinase, p-STAT3, and NF-κB. These effects were blocked by MAPK inhibitors and N-acetyl-L-cysteine. Furthermore, 10-HDA inhibited cell migration by regulating transforming growth factor beta 1 (TGF-β1), SNAI1, GSK-3β, E-cadherin, N-cadherin, and vimentin. Taken together, the results of this study showed that 10-HDA induced cell cycle arrest and apoptosis in A549 human lung cancer cells through ROS-mediated MAPK, STAT3, NF-κB, and TGF-β1 signaling pathways. Therefore, 10-HDA may be a potential therapy for human lung cancer.

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

scholarly journals KLF8 overexpression promotes the growth of human lung cancer cells by promoting the expression of JMJD2A

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Dongjie Ma ◽  
Hongsheng Liu ◽  
Yingzhi Qin ◽  
Zhenhuan Tian ◽  
Shanqing Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Colony Formation ◽  
Human Lung ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Small Cell Lung

Abstract Background Non-small-cell lung cancer (lung cancer) has become one of the leading causes worldwide and the underlying mechanism is not fully understood. The transcriptional factor Kruppel like factor 8 (KLF8) is involved in the initiation, progression, transformation, and metastasis of diverse cancers. However, the roles of KLF8 in human non-small cell lung cancer remain unknown. Methods CCK-8 kit and colony formation assay were performed to determine the cell growth of lung cancer cells. Flow cytometry analysis was used to evaluate apoptosis and cell cycle of lung cancer cells. Luciferase reporter assay was used to examine the activation of JMJD2A promoter by KLF8. Chromatin immunoprecipitation assay was performed to evaluate the binding of KLF8 to JMJD2A promoter. Western blot and polymerase chain reaction were applied to analyze the expression of interested genes. Results The mRNA and protein levels of KLF8 in human non-small cell lung cancer tissues were overexpressed compared with the non-cancer tissues. KLF8 was knocked down with lentivirus-mediated short-hairpin RNA (shRNA) in human lung cancer cells (A549 and H1299 cells). The phenotypic results showed that KLF8 knockdown decreased the proliferation rate and colony formation of lung cancer cells. By contrast, lentivirus-mediated KLF8 overexpression promoted the growth of lung cancer cells (A549 and H1299 cells) and non-cancerous bronchial epithelial cell line BEAS-2B. Next, we showed that KLF8 regulated cell cycle at the G0 phase but not regulates cellular apoptosis of lung cancer cells. KLF8 regulated the expression of the cell cycle regulators P21 and CDK4 in a JMJD2A-dependent manner and JMJD2A knockdown significantly blocked the functions of KLF8 in regulating cell cycle and proliferation of lung cancer cells. Finally, we observed that KLF8 bound the promoter of JMJD2A and facilitated the expression of JMJD2A. Conclusions Our evidence demonstrated that KLF8 upregulation in human lung cancer promotes the cell proliferation and colony formation of lung cancer cells. KLF8 binds to the promoter of JMJD2A and subsequently regulates the expression of P21 and CDK4, which contributes to the regulation of cell cycle by KLF8. KLF8 may serve as a target for the treatment of human lung cancer.

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