scholarly journals The DEAD-box RNA helicase 51 controls non-small cell lung cancer proliferation by regulating cell cycle progression via multiple pathways

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaojing Wang ◽  
Hongli Liu ◽  
Chengling Zhao ◽  
Wei Li ◽  
Huanbai Xu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Progression ◽  
Rna Helicase ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cancer Proliferation ◽  
Cycle Progression ◽  
Dead Box

Validation of a cell cycle progression score for 5-year mortality risk in patients with stage I non-small cell lung cancer.

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. 7522-7522
Author(s):  
Takashi Eguchi ◽  
Kadota Kyuichi ◽  
Brent Evans ◽  
Camelia S. Sima ◽  
Thaylon Davis ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Mortality Risk ◽  
Cell Cycle Progression ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Progression ◽  
A Cell

scholarly journals Quinacrine Overcomes Resistance to Erlotinib by Inhibiting FACT, NF-κB, and Cell-Cycle Progression in Non–Small Cell Lung Cancer

2014 ◽  
Vol 13 (9) ◽  
pp. 2203-2214 ◽  
Author(s):  
Josephine Kam Tai Dermawan ◽  
Katerina Gurova ◽  
John Pink ◽  
Afshin Dowlati ◽  
Sarmishtha De ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Cycle Progression ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Progression

scholarly journals Deubiquitinase DUB3 Regulates Cell Cycle Progression via Stabilizing Cyclin A for Proliferation of Non-Small Cell Lung Cancer Cells

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 297 ◽  
Author(s):  
Bin Hu ◽  
Tanggang Deng ◽  
Hongchang Ma ◽  
Yan Liu ◽  
Peifu Feng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Cycle Progression ◽  
Critical Role ◽  
Cyclin A ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Progression

The deubiquitinase DUB3 is frequently overexpressed in non-small cell lung cancer (NSCLC) and contributes to its malignant phenotype. However, the underlying molecular mechanism of DUB3 in NSCLC is largely unknown. In this study, we report that DUB3 regulates cell cycle progression by deubiquitinating cyclin A that links to proliferation of NSCLC cells. We found that knockdown of DUB3 decreases cyclin A levels, whereas overexpression of DUB3 strongly increases cyclin A levels. Mechanistically, DUB3 interacts with cyclin A, which removes the polyubiquitin chains conjugated onto cyclin A and stabilizes the cyclin A protein. Furthermore, we demonstrate that DUB3 regulates cell cycle progression by stabilizing cyclin A, because ablation of DUB3 arrests cell cycle from G0/G1 to S phase and the resulting effect can be rescued by introducing cyclin A into NSCLC cells. Functionally, we found that the effect of DUB3 on cyclin A mediates proliferation of NSCLC cells. Moreover, a significant correlation between DUB3 abundance and cyclin A expression levels were also found in NSCLC samples. Taken together, these results reveal that DUB3 functions as a novel cyclin A regulator through maintaining cyclin A stability, and that the DUB3-cyclin A signaling axis plays a critical role in cell cycle progression for proliferation of NSCLC.

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