Nanjing, China

Nanjing University

www.nju.edu.cn
Nanjing, China

Nanjing University , or Nanking University, is one of the oldest and most prestigious institutions of higher learning in China. Following many changes through dynasties since CE 258, it was established as a modern school in 1902 in late Qing dynasty, and became a modern university in the early 1920s, the early years of Republic of China, being the first Chinese modern university with the combination of education and research, and also as a pioneer laying the foundations for the establishment of the modern educational system in China. Before the eve of establishment of People's Republic of China in 1949, the name was changed from National Central University to Nanjing University.Nanjing University is a comprehensive research university. It is a member of the C9 League and Yangtze Delta Universities Alliance. NJU is a national university directly under the Ministry of Education of China, largely financed by the national and the Jiangsu provincial governments. Nanjing University has two campuses: Gulou campus, located in the centre of Nanjing, and Xianlin campus, located in northeast of Nanjing south of the Yangtze River, which is the home to most undergraduate students and graduate students of several departments. Wikipedia.


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PubMed | Aurora University, Huzhou Central Hospital and Nanjing University
Type: | Journal: Scientific reports | Year: 2016

Long noncoding RNA (lncRNA) plays pivotal roles in cancer development. To date, only a small number of lncRNAs have been characterized at functional level. Here, we discovered a novel lncRNA termed GAS5-AS1 as a tumor suppressor in non-small cell lung cancer (NSCLC). The expression of GAS5-AS1 in NSCLC tumors was much lower than that in the adjacent normal lung tissues. The reduced GAS5-AS1 was significantly correlated with larger tumors, higher TNM stages, and lymph node metastasis in NSCLC patients. While ectopic expression or specific knockdown of GAS5-AS1 had no effect on proliferation, cell cycle progression, and apoptosis, it dramatically decreased or increased, respectively, NSCLC cell migration and invasion. Overexpression of GAS5-AS1 in NSCLC cells reduced a cohort of molecules (ZEB1, N-cadherin, Vimentin, and/or Snail1) critical for epithelial-mesenchymal transition (EMT). Furthermore, the DNA demethylating agent 5-aza-2-deoxycytidine failed to upregulate GAS5-AS1 in NSCLC cells, whereas the pan-HDAC inhibitors panobinostat and SAHA significantly induced GAS5-AS1 in a dose-dependent manner. In addition, GAS5-AS1 can be upregulated by specific knockdown of HDAC1 or HDAC3. Collectively, our data suggest that histone modifications play a major role leading to epigenetic silencing of GAS5-AS1 in NSCLC and subsequently promote tumor metastasis via upregulation of several key EMT markers.

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