Low Wilms’ Tumor Gene Expression in Tumor Tissues Predicts Poor Prognosis in Patients with Non-Small-Cell Lung Cancer

2012 ◽  
Vol 30 (2) ◽  
pp. 165-171 ◽  
Author(s):  
Seiji Hayashi ◽  
Yusuke Oji ◽  
Yuko Kanai ◽  
Tomoaki Teramoto ◽  
Masanori Kitaichi ◽  
...  
2020 ◽  
Author(s):  
Wenbin Wu ◽  
Cheng Fang ◽  
Chaochao Zhang ◽  
Nanhua Hu ◽  
Lixin Wang

Abstract Background: The lung cancer has become the most lethal cause of cancer-related death in China and is responsible for more than 1 million deaths all of the world every year, especially non-small cell lung cancer (NSCLC). Although great advance in pharmaceutical therapies for lung cancer patients, the overall survival is still poor. It is necessary to find out the effective biomarkers in order to improve and predict the prognosis of lung cancer patients. The integrated bioinformatical analysis, as a useful tool to dig up the valuable clues, can be applied to search new effective therapeutic targets. Methods: In this work, we utilized four NSCLC datasets (GSE18842, GSE31210, GSE33532 and GSE101929) from Gene Expression Omnibus (GEO) to analyze. We totally found that there were 162 differentially expressed genes (DEGs) in these four datasets, including 41 up-regulated genes and 121 down-regulated genes in NSCLC tissues. The analysis of GO enrichment and KEGG pathway was done by DAVID software. Then, we identified 10 core oncogenes by constructing protein-protein interaction (PPI) network. Last, we further analyzed the 10 core oncogenes through Kaplan Meier plotter online database and Gene Expression Profiling Interactive Analysis (GEPIA) respectively. Results: We discovered 10 key oncogenes which were associated with the progression and poor prognosis for NSCLC, including ANLN, CCNA2, CDCA7, DEPDC1, DLGAP5, HMMR, KIAA0101, RRM2, TOP2A, and UBE2T. Conclusion: These 10 genes can be served as the therapeutic targets and useful prognostic biomarkers for NSCLC treatment.


2018 ◽  
Vol 64 (4) ◽  
pp. 522-527
Author(s):  
Aleksey Shutko ◽  
Viktor Mus

Individual parameters of circulating hemopoietic stem cells (HSC) lymphoid origin were measured by cytofluorometry before treatment of patients with metastatic non-small cell lung cancer and were retrospectively compared with individual life span's (LS). The possibility of poor prognosis of treatment's results (LS


Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 3426-3433
Author(s):  
Juanjuan Yong ◽  
Liyun Huang ◽  
Gengbiao Chen ◽  
Xiaoya Luo ◽  
Hui Chen ◽  
...  

2017 ◽  
Vol 14 (4) ◽  
pp. 3959-3966 ◽  
Author(s):  
Dan Liu ◽  
Yi Huang ◽  
Li Zhang ◽  
Dong-Ni Liang ◽  
Li Li

Lung Cancer ◽  
2000 ◽  
Vol 29 (1) ◽  
pp. 193
Author(s):  
M Higashiyama ◽  
K Kodama ◽  
H Yokouchi ◽  
K Takami ◽  
Y Miyoshi ◽  
...  

2018 ◽  
Vol 45 (6) ◽  
pp. 2213-2224 ◽  
Author(s):  
Meng Zhao ◽  
Yahui Liu ◽  
Ran Liu ◽  
Jin Qi ◽  
Yongwang Hou ◽  
...  

Background/Aims: Cytokines are key players in tumorigenesis and are potential targets in cancer treatment. Although IL-6 has attracted considerable attention, interleukin 11 (IL-11), another member of the IL-6 family, has long been overlooked, and little is known regarding its specific function in non-small cell lung cancer (NSCLC). In this study, we explored IL-11’s role in NSCLC and the detailed mechanism behind it. Methods: Cell proliferation in response to IL-11 was determined by colony formation, BrdU incorporation and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Cell motility was measured by Transwell and wound healing assays. NSCLC xenograft models were used to confirm oncogenic function of IL-11 in vivo. Immunohistochemical staining and western blot assay were performed to detect epithelial–mesenchymal transition (EMT) markers and cell signaling pathway alterations. Eighteen NSCLC patients and 5 normal lung samples were collected together with data from an online database to determine the link between IL-11 expression and malignant progression. Results: We observed that IL-11 was upregulated in NSCLC samples compared with normal tissue samples and correlated with poor prognosis. Data from in vitro and in vivo models indicated that IL-11 promotes cell proliferation and tumorigenesis. Cell migration and invasion were also enhanced by IL-11. Epithelial–mesenchymal transition (EMT) was also observed after IL-11 incubation. Furthermore, IL-11 activated AKT and STAT3 in our experimental models. In addition, we observed that hypoxia induced IL-11 expression in NSCLC cells. Deferoxamine (DFX) or dimethyloxalylglycine (DMOG) induced hypoxia-inducible factor 1-alpha (HIF1α) upregulation, which enhanced IL-11 expression in NSCLC cells. Conclusions: Taken together, our results indicate that IL-11 is an oncogene in NSCLC, and elucidating the mechanism behind it may provide insights for NSCLC treatment.


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