单位：[1]Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang, China[2]Department of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China[3]Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China[4]Department of Stomatology, The Second Hospital of Hebei Medical University, Shijiazhuang, China[5]Department of Pathology, China‐Japan Friendship Hospital, Beijing, China[6]Department of Molecular, Cellular and Development Biology, University of Colorado Boulder, Boulder, USA[7]Laboratory of Pathology, Hebei Medical University, Shijiazhuang, China
Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1 in carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has not been characterized. In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)-96 and effectively function as a sponge for miR-96, thus antagonizing the functions of miR-96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR-96 and regulate KRAS expression, which highlights the importance of the complicated miRNA-lncRNA network in modulating the progression of PDAC.
基金：
Scientific Research Foundation from Public Health Department of Hebei province, China [20170556]; National Nature Science Foundations of ChinaNational Natural Science Foundation of China (NSFC) [81472326, 81702299]; Natural Science Foundation of Hebei province, ChinaNatural Science Foundation of Hebei Province [H2017206022]
第一作者单位：[1]Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang, China
共同第一作者：
通讯作者：
通讯机构：[1]Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang, China[2]Department of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China[3]Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China[*1]Department of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China[*2]Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.[*3]Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
推荐引用方式(GB/T 7714)：
Zhang Yufeng,Yang Haiyan,Du Yong,et al.Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA-96[J].CANCER SCIENCE.2019,110(9):2760-2772.doi:10.1111/cas.14136.
APA：
Zhang, Yufeng,Yang, Haiyan,Du, Yong,Liu, Pingping,Zhang, Jing...&Zhang, Xianghong.(2019).Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA-96.CANCER SCIENCE,110,(9)
MLA：
Zhang, Yufeng,et al."Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA-96".CANCER SCIENCE 110..9(2019):2760-2772
