scholarly journals Survival-based bioinformatics analysis to identify hub genes and key pathways in non-small cell lung cancer

2019 ◽  
Vol 8 (4) ◽  
pp. 1188-1198
Author(s):  
Chunliang Liu ◽  
Yu Chen ◽  
Yuqi Deng ◽  
Yu Dong ◽  
Jixuan Jiang ◽  
...  
2020 ◽  
Vol 9 (11) ◽  
pp. 7149-7164
Author(s):  
Yu Zeng ◽  
Nanhong Li ◽  
Riken Chen ◽  
Wang Liu ◽  
Tao Chen ◽  
...  

Aging ◽  
2020 ◽  
Vol 12 (18) ◽  
pp. 17948-17957
Author(s):  
Jianlong Bu ◽  
Pinyi Zhang ◽  
Kaibin Zhu ◽  
Yubo Yan ◽  
Bowen Shi ◽  
...  

2017 ◽  
Vol 14 (1) ◽  
pp. 58-77
Author(s):  
Sevgi Gezici ◽  
Mehmet Ozaslan ◽  
Gurler Akpinar ◽  
Murat Kasap ◽  
Maruf Sanli ◽  
...  

2019 ◽  
Vol 121 (3) ◽  
pp. 2690-2703 ◽  
Author(s):  
Feifeng Song ◽  
Zixue Xuan ◽  
Xiuli Yang ◽  
Xiaolan Ye ◽  
Zongfu Pan ◽  
...  

2020 ◽  
Vol 50 (9) ◽  
pp. 1058-1067 ◽  
Author(s):  
Ying Chen ◽  
Tianle Shen ◽  
Xuping Ding ◽  
Lei Cheng ◽  
Liming Sheng ◽  
...  

Abstract Introduction Non-small cell lung cancer was one of the most common and deadly cancers worldwide. Long non-coding RNAs had been implicated in multiple human cancers, including non-small cell lung cancer. In this study, we focused on a novel long non-coding RNA, HAGLROS, in non-small cell lung cancer. Material and methods In this study, we used GEPIA dataset to analyse the expression levels of HAGLROS in non-small cell lung cancer samples and normal tissues. Then, we analysed Kaplan–Meier Plotter database to reveal the association between HAGLROS expression and overall survival time in patients with non-small cell lung cancer. Moreover, we used small interfering RNA-mediated knockdown to reduce HAGLROS expression in A549 and H1299 cells. Cell Counting Kit-8 assay was used to detect the effect of HAGLROS on cell proliferation. Transwell assays were used to determine the effect of HAGLROS on cell migration and invasion. Co-expression analysis and bioinformatics analysis were conducted to predict the potential functions of HAGLROS in non-small cell lung cancer. Results We identified HAGLROS was significantly overexpressed in non-small cell lung cancer samples compared to normal tissues. Higher expression of HAGLROS was significantly associated with shorter overall survival time in patients with non-small cell lung cancer. Moreover, we found knockdown of HAGLROS in non-small cell lung cancer cells remarkably suppressed tumour proliferation, migration and invasion. By conducting bioinformatics analysis, we found HAGLROS was involved in regulating multiple cancer-related pathways, including Spliceosome, DNA replication, cell cycle, chromosome segregation and sister chromatid segregation. Conclusions Our results for the first time demonstrated HAGLROS may serve as a target for new therapies in non-small cell lung cancer.


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