Peroxisome Proliferator-Activated Receptor-γ Is a Target of Nonsteroidal Anti-Inflammatory Drugs Mediating Cyclooxygenase-Independent Inhibition of Lung Cancer Cell Growth

2002 ◽  
Vol 62 (5) ◽  
pp. 1207-1214 ◽  
Author(s):  
Marilee Wick ◽  
Greg Hurteau ◽  
Christina Dessev ◽  
Daniel Chan ◽  
Mark W. Geraci ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Peroxisome Proliferator ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Peroxisome Proliferator Activated Receptor ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

scholarly journals Peroxisome proliferator-activated receptor δ as a molecular target to regulate lung cancer cell growth

FEBS Letters ◽  
2005 ◽  
Vol 579 (17) ◽  
pp. 3829-3836 ◽  
Author(s):  
Keiko Fukumoto ◽  
Yoshihisa Yano ◽  
Nantiga Virgona ◽  
Hiromi Hagiwara ◽  
Hiromi Sato ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Molecular Target ◽  
Peroxisome Proliferator ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Peroxisome Proliferator Activated Receptor

USP10 inhibits lung cancer cell growth and invasion by upregulating PTEN

2017 ◽  
Vol 441 (1-2) ◽  
pp. 1-7 ◽  
Author(s):  
Jia Sun ◽  
Tianxiang Li ◽  
Yinying Zhao ◽  
Lirong Huang ◽  
Hua Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

CHML targeted by miR-199a-3p promotes non-small cell lung cancer cell growth via binding to Rab5A

2021 ◽  
pp. 153626
Author(s):  
Changqing Dong ◽  
Hui Cao ◽  
Zhengcheng Liu ◽  
Lei Xi ◽  
Ye Shi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Cancer Cell Growth

scholarly journals FBXO22 mediates polyubiquitination and inactivation of LKB1 to promote lung cancer cell growth

2019 ◽  
Vol 10 (7) ◽  
Author(s):  
Xiao-Na Zhu ◽  
Ping He ◽  
Liang Zhang ◽  
Shuo Yang ◽  
Hui-Lin Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

Cyclin D1 antisense RNA destabilizes pRb and retards lung cancer cell growth

1997 ◽  
Vol 273 (5) ◽  
pp. L941-L949 ◽  
Author(s):  
Barbara Driscoll ◽  
Lingtao Wu ◽  
Susan Buckley ◽  
Frederick L. Hall ◽  
Kathryn D. Anderson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cyclin D ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Transfected Cells ◽  
The Impact

To investigate the role of cyclin D1 in the regulation of lung cancer cell growth, we created five stably transfected cell lines carrying a cyclin D1 antisense construct. The transfected cells exhibited a marked decrease in the rate of cell growth, in contrast to the original lines (A549 and NCI-H441). The expression of several cell cycle-regulating proteins, including cyclin A, the cyclin-dependent kinases (cdk) 2 and cdk4, in addition to cyclin D1 itself, was markedly decreased. The expression of one cdk inhibitor, p21WAF1/CIP1, increased in the A549-derived cell lines. A specific target of cyclin D1 activity, the growth-suppressing product of the retinoblastoma gene, pRb, exhibited decreased expression and a decreased level of phosphorylation in the transfected cells. Decreased expression of pRb due to a significant increase in its turnover rate suggested that the stability of the protein may depend on phosphorylation by cyclin D1-dependent cdk activity. In addition to the impact on pRb stability, decreased expression of cyclin D1 induced susceptibility to cell death after withdrawal of exogenous growth factors in the antisense transfected cell lines, a response that was not observed in the original cancer cell lines. We conclude that abrogation of cyclin D1 overexpression in lung cancer cells disrupts several key pathways that are required for uncontrolled cell growth and induces those that lead to cell death after growth factor deprivation. Therefore, we speculate that use of antisense cyclin D1 expression in appropriate gene vectors could be a useful method for retarding lung cancer cell growth in accessible tumors such as those of the lung epithelium.

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