scholarly journals Retraction notice to “Down-regulation of lncRNA ADAMTS9-AS2 contributes to gastric cancer development via activation of PI3K/Akt pathway” [Biomed. Pharmacother. 107 (2018) 185–193]

2021 ◽  
Vol 142 ◽  
pp. 112116
Author(s):  
Bole Cao ◽  
Cuixia Liu ◽  
Guifeng Yang
2019 ◽  
Vol 120 (8) ◽  
pp. 13903-13911 ◽  
Author(s):  
Xuekui Wang ◽  
Shen Gao ◽  
Feng Xie ◽  
Wei Li ◽  
Miyang Li ◽  
...  

2018 ◽  
Vol 19 (12) ◽  
pp. 3881 ◽  
Author(s):  
Kobra Foroughi ◽  
Mohammad Amini ◽  
Amir Atashi ◽  
Habibollah Mahmoodzadeh ◽  
Ute Hamann ◽  
...  

Gastric cancer (GC) is the fifth most common cancer and the third most frequent cause of cancer deaths worldwide. The high death rate associated with GC, and lack of appropriate biomarkers for diagnosis, prognosis, and treatment emphasize the need for identification of novel molecules. Given the emerging roles for long non-coding RNAs (lncRNAs) in cancer development, we studied novel lncRNA candidates involved in gastric carcinogenesis. LncRNA candidate discovery was performed using analyses of available datasets and literature. Validation was done using an internal sample set of GC/normal tissues, and external independent datasets. Network analysis and functional annotation of co-expressed protein coding genes were performed using the weighted gene correlation network analysis (WGCNA) and ingenuity pathway analysis. Two novel lncRNAs, PCAT18 and LINC01133, associated with GC development were identified by analysis of the discovery Gene Expression Omnibus (GEO) datasets. The down-regulation of these genes in GC tissues was successfully validated internally and externally. The results showed a tissue-specific down-regulation of PCAT18 and LINC01133 in gastrointestinal tissues. WGCNA and ingenuity pathway analyses revealed that the genes co-expressed with the two lncRNAs were mostly involved in metabolic pathways and networks of gastrointestinal disease and function. Our findings of a tissue-specific down-regulation of PCAT18 and LINC01133 in gastric and other gastrointestinal cancers imply that these lncRNAs may have a tumor suppressive function in the development of these tumor entities. The two lncRNA biomarkers may contribute to a better understanding of the complex mechanisms of gastric carcinogenesis.


2020 ◽  
Vol 126 ◽  
pp. 109941 ◽  
Author(s):  
Hu Song ◽  
Yixin Xu ◽  
Teng Xu ◽  
Ruizhi Fan ◽  
Tao Jiang ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (38) ◽  
pp. 63813-63824 ◽  
Author(s):  
Ying Chen ◽  
Guoqing Wei ◽  
Hongwei Xia ◽  
Huangfei Yu ◽  
Qiuling Tang ◽  
...  

2005 ◽  
Vol 65 (7) ◽  
pp. 2746-2754 ◽  
Author(s):  
Daoyan Wei ◽  
Weida Gong ◽  
Masashi Kanai ◽  
Christian Schlunk ◽  
Liwei Wang ◽  
...  

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 181
Author(s):  
Masami Suganuma ◽  
Tatsuro Watanabe ◽  
Eisaburo Sueoka ◽  
In Kyoung Lim ◽  
Hirota Fujiki

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.


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