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
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Pin-Dong Li1,2,*, Jian-Li Hu1,*, Charlie Ma2, Hong Ma1, Jing Yao1, Li-Li Chen2, Jing Chen1, Tian-Tian Cheng3, Kun-Yu Yang1, Gang Wu1, Wen-Jie Zhang4 and Ru-Bo Cao1
1Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
2Department of Radiation Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA
3Cancer Center of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong 510059, China
4Department of Pathology, Shihezi University School of Medicine, Shihezi, Xinjiang 832002, China
*These authors have contributed equally to this work
Ru-Bo Cao, email: email@example.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
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.
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