scholarly journals A novel seven-long non-coding RNA signature predicts survival in early stage lung adenocarcinoma

Oncotarget ◽  
2017 ◽  
Vol 8 (9) ◽  
pp. 14876-14886 ◽  
Author(s):  
Mingwei Chen ◽  
Baoquan Liu ◽  
Jianbing Xiao ◽  
Yingnan Yang ◽  
Yafang Zhang
Oncotarget ◽  
2016 ◽  
Vol 7 (20) ◽  
pp. 29720-29738 ◽  
Author(s):  
Meng Zhou ◽  
Wanying Xu ◽  
Xiaolong Yue ◽  
Hengqiang Zhao ◽  
Zhenzhen Wang ◽  
...  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  

Abstract Background Although using a blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism and efficacy of such immune-checkpoint inhibition strategies in solid tumors remains unclear. Results Employing qRT-PCR, Sanger sequencing, and RNA BaseScope analysis, we show that human lung adenocarcinoma (LUAD) all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) by alternative splicing, regardless if the tumor is positive or negative for the protein PD-L1. Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity. Conclusions In summary, the PD-L1 gene can generate a long non-coding RNA through alternative splicing to promote lung adenocarcinoma progression by enhancing c-Myc activity. Our results argue in favor of investigating PD-L1-lnc depletion in combination with PD-L1 blockade in lung cancer therapy.


2016 ◽  
Vol 35 (6) ◽  
pp. 3185-3197 ◽  
Author(s):  
CHUNLIANG SHANG ◽  
WENHUI ZHU ◽  
TIANYU LIU ◽  
WEI WANG ◽  
GUANGXIN HUANG ◽  
...  

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