Shandong University scholars have discovered a long-chain non-coding RNA that activates the progression of gastric cancer cell cycle
Shandong University scholars have discovered a long-chain non-coding RNA that activates the progression of gastric cancer cell cycle
October 12, 2018 Source: Ministry of Science and Technology
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];Recently, Professor Gao Peng from the Basic Medical College of Shandong University found that EGR1-mediated long-chain non-coding RNA transcription can activate cell cycle progression in gastric cancer, and EGR1-activated HNF1A-AS1 regulates various growth-promoting and anti-growth factors. Thereby promoting the occurrence and development of gastric cancer, can be used as a therapeutic target. An article entitled "EGR1-mediated transcription of lncRNA-HNF1A-AS1 promotes cell cycle progression in gastric cancer" was published in the journal Cancer Research.
Gastric cancer is one of the three major causes of cancer-related deaths in the world. China is a high incidence area for gastric cancer. It is of great significance to conduct in-depth research on the mechanism of gastric carcinogenesis to determine potential therapeutic targets and to seek effective treatment methods to improve patient survival.
Professor Gao Peng's research team found that hepatocyte nuclear factor 1 homologous protein A antisense RNA 1 (HNF1A-AS1) was up-regulated in gastric cancer tissues, and early growth response protein 1 (EGR1) binds to the HNF1A-AS1 promoter region, activating its transcription and Promote the proliferation of gastric cancer cells. At the same time, the researchers found in the mechanism study that HNF1A-AS1 acts as an endogenous competitive RNA to up-regulate the expression of miR-661 direct target cell division cycle 34 (CDC34) by adsorption of miR-661.
In addition, EGR1 and HNF1A-AS1 inhibited the expression of p21 by promoting CDC34-mediated p21 ubiquitination, thereby enhancing cyclin expression, and EGR1-activated HNF1A-AS1 regulates various growth-promoting factors and anti-growth factor promotion. The occurrence and development of gastric cancer can be used as a target for treatment.
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