scholarly journals Inhibition of human lung cancer proliferation through targeting stromal fibroblasts by dihydromyricetin

2017 ◽  
Vol 16 (6) ◽  
pp. 9758-9762 ◽  
Author(s):  
Kai-Jie Fan ◽  
Bo Yang ◽  
Yang Liu ◽  
Xiao-Dong Tian ◽  
Bo Wang
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Cancer Proliferation ◽  
Stromal Fibroblasts

scholarly journals PEG10 plays a crucial role in human lung cancer proliferation, progression, prognosis and metastasis

2014 ◽  
Vol 32 (5) ◽  
pp. 2159-2167 ◽  
Author(s):  
XINZHOU DENG ◽  
YI HU ◽  
QIANSHAN DING ◽  
RONGFEI HAN ◽  
QIAN GUO ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Crucial Role ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Cancer Proliferation

Ras Denitrosylation in Human Lung Cancer

2012 ◽  
Vol 3 (2) ◽  
pp. 135-139
Author(s):  
Benjamin Gaston ◽  
Nadzeya Marozkina
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Human Lung Cancer

MicroRNAs expression signature in human lung cancer cell

2014 ◽  
Author(s):  
Geyu Liang ◽  
Xikai Wang ◽  
Yanqiu Zhang ◽  
Yanyun Fu ◽  
Lihong Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Human Lung Cancer Cell ◽  
Expression Signature

Inhibitory effects of Actinidia Chinensis planch root extracts (acRoots) on human lung cancer cells through retinoic acid receptor beta

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Lingyan Wang ◽  
Jiayun Hou ◽  
Minghuan Zheng ◽  
Lin Shi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Retinoic Acid Receptor ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Inhibitory Effects ◽  
The Core ◽  
Human Lung Cancer Cells ◽  
Receptor Beta

Actinidia Chinensis Planch roots (acRoots) are used to treat many cancers, although the anti-tumor mechanism by which acRoots inhibit cancer cell growth remains unclear. The present study aims at investigating inhibitory effects of acRoots on human lung cancer cells and potential mechanisms. Our data demonstrate that the inhibitory effects of acRoots on lung cancer cells depend on genetic backgrounds and phenotypes of cells. We furthermore found the expression of metabolism-associated gene profiles varied between acRoots-hypersensitive (H460) or hyposensitive lung cancer cells (H1299) after screening lung cancer cells with different genetic backgrounds. We selected retinoic acid receptor beta (RARB) as the core target within metabolism-associated core gene networks and evaluated RARB changes and roles in cells treated with acRoots at different concentrations and timeframes. Hypersensitive cancer cells with the deletion of RARB expression did not response to the treatment with acRoots, while RARB deletion did not change effects of acRoots on hyposensitive cells. Thus, it seems that RARB as the core target within metabolism-associated networks plays important roles in the regulation of lung cancer cell sensitivity to acRoots.

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