Long noncoding RNA uc.345 promotes tumorigenesis of pancreatic cancer by upregulation of hnRNPL expression
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Chao Liu1,2,*, Jiamin Wang3,4,*, Xiaoyuan Yuan3,4, Wenli Qian3,4, Bosen Zhang1, Minmin Shi2, Junjie Xie1, Baiyong Shen1,2, Hong Xu3,4, Zhaoyuan Hou3,4,5, Hao Chen1,2
1Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
2Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
3Hongqiao Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China
4Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiaotong University School of Medicine, Shanghai, China
5Key Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China
*These authors contributed equally to this paper
Hong Xu, email: email@example.com
Hao Chen, email: firstname.lastname@example.org
Zhaoyuan Hou, email: email@example.com
Keywords: pancreatic cancer, lncRNA, uc.345, cancer stem cells, hnRNPL
Received: February 10, 2016 Accepted: September 20, 2016 Published: September 26, 2016
Increasing evidence points to an important functional or regulatory role of long noncoding RNA in cellular processes as well as cancer diseases resulted from the aberrant lncRNA expression. LncRNA could participate in the cancer progression and develop a significant role through the interaction with proteins. In the present study, we report a lncRNA termed uc.345 that is up-regulated in tumor tissues, compared to the corresponding noncancerous tissues. We found that a higher uc.345 expression level was more frequently observed in tissues with increased depth of invasion and advanced TNM tumor node metastasis T stage. Moreover, uc.345 could be used as an independent risk factor for the overall survival (OS) of the pancreatic cancer patients. By employing soft agar assays and tumor xenograft models, we showed that uc.345 could accelerate tumor growth. Further, we discovered that uc.345 could upregulate the hnRNPL expression and that inhibition of (hnRNPL) dampens the tumorigenesis capability of uc.345. Collectively, these results demonstrate that uc.345 functions as an oncogenic lncRNA that promotes tumor progression and serves as a poor predictor for pancreatic cancer patients’ overall survival.
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