Upregulation of the long non-coding RNA PVT1 promotes esophageal squamous cell carcinoma progression by acting as a molecular sponge of miR-203 and LASP1

Abstract

// Pin-Dong Li 1, 2, * , Jian-Li Hu 1, * , Charlie Ma 2 , Hong Ma 1 , Jing Yao 1 , Li-Li Chen 2 , Jing Chen 1 , Tian-Tian Cheng 3 , Kun-Yu Yang 1 , Gang Wu 1 , Wen-Jie Zhang 4 and Ru-Bo Cao 1 1 Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 2 Department of Radiation Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA 3 Cancer Center of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong 510059, China 4 Department of Pathology, Shihezi University School of Medicine, Shihezi, Xinjiang 832002, China * These authors have contributed equally to this work Correspondence to: Ru-Bo Cao, email: caorubao@126.com Keywords: long non-coding RNA, PVT1, LASP1, miR-203, esophageal squamous cell carcinoma Received: November 01, 2016      Accepted: January 16, 2017      Published: March 03, 2017 ABSTRACT Long non-coding RNAs are a group of non-coding RNAs longer than 200 nucleotides and possess diverse functions and exhibit exquisite cell-specific and developmental dynamic expression patterns. The role of the long non-coding RNA PVT1 in esophageal squamous cell carcinoma remains unsolved. Here, we showed that PVT1 expression is significantly up-regulated in ESCC tumor samples compared with their normal counterparts. Knockdown of PVT1 suppressed tumor growth in vitro and in vivo . Further studies revealed that silence of PVT1 lead to up-regulation of miR-203, and vice versa. Moreover, LASP1 was found to be downregulated after knockdown of PVT1 and overexpression of LASP1 attenuated the tumor-suppressive roles of PVT1 knockdown. Our results suggest that PVT1 promote ESCC progression via functioning as a molecular sponge for miR-203 and LASP1 and provide the first evidence of dysregulated PVT1/miR-203/LASP1 axis in ESCC.