scholarly journals Loss of function of SWI/SNF chromatin remodeling genes leads to genome instability of human lung cancer

2014 ◽  
Vol 33 (1) ◽  
pp. 283-291 ◽  
Author(s):  
HAI-TAO HUANG ◽  
SHAO-MU CHEN ◽  
LIANG-BIN PAN ◽  
JIE YAO ◽  
HAI-TAO MA
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xiaohong Tan ◽  
Lu Tong ◽  
Lin Li ◽  
Jinjin Xu ◽  
Shaofang Xie ◽  
...  

AbstractSMAD4 is mutated in human lung cancer, but the underlying mechanism by which Smad4 loss-of-function (LOF) accelerates lung cancer metastasis is yet to be elucidated. Here, we generate a highly aggressive lung cancer mouse model bearing conditional KrasG12D, p53fl/fl LOF and Smad4fl/fl LOF mutations (SPK), showing a much higher incidence of tumor metastases than the KrasG12D, p53fl/fl (PK) mice. Molecularly, PAK3 is identified as a downstream effector of Smad4, mediating metastatic signal transduction via the PAK3-JNK-Jun pathway. Upregulation of PAK3 by Smad4 LOF in SPK mice is achieved by attenuating Smad4-dependent transcription of miR-495 and miR-543. These microRNAs (miRNAs) directly bind to the PAK3 3′UTR for blockade of PAK3 production, ultimately regulating lung cancer metastasis. An inverse correlation between Smad4 and PAK3 pathway components is observed in human lung cancer. Our study highlights the Smad4-PAK3 regulation as a point of potential therapy in metastatic lung cancer.


Author(s):  
Benjamin Gaston ◽  
Nadzeya Marozkina

Author(s):  
Geyu Liang ◽  
Xikai Wang ◽  
Yanqiu Zhang ◽  
Yanyun Fu ◽  
Lihong Yin ◽  
...  

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Lingyan Wang ◽  
Jiayun Hou ◽  
Minghuan Zheng ◽  
Lin Shi

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.


2011 ◽  
Vol 31 (10) ◽  
pp. 1091-1095
Author(s):  
Xiao-lin LI ◽  
Yan-fang ZHANG ◽  
Kai TANG ◽  
Ying TANG ◽  
Ruo-bing JIN ◽  
...  

Author(s):  
Mohammad Lalmoddin Mollah ◽  
Jae-Chan Song ◽  
Chang-Ho Park ◽  
Gee-Dong Lee ◽  
Joo-Heon Hong ◽  
...  

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