LINC00052 upregulates EPB41L3 to inhibit migration and invasion of hepatocellular carcinoma by binding miR-452-5p

// Liying Zhu 1, 3, * , Nenghong Yang 4, * , Juan Chen 1 , Tao Zeng 1 , Shaoying Yan 1 , Yuyang Liu 1 , Gangfeng Yu 1 , Qiuxu Chen 1 , Guiqin Du 3 , Wei Pan 3 , Xing Li 3 , Huihao Zhou 1 , Ailong Huang 1, 2 and Hua Tang 1 1 Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China 2 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, China 3 Department of Medical Laboratory, Guizhou Medical University, Guiyang, China 4 Department of Hepatobiliary Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, China * These authors have contributed equally to this work Correspondence to: Hua Tang, email: tanghua86162003@cqmu.edu.cn Ailong Huang, email: ahuang1964@163.com Keywords: HCC, LINC00052, EPB41L3, migration, invasion Received: March 22, 2017 Accepted: June 05, 2017 Published: June 29, 2017 ABSTRACT Numerous studies have demonstrated that a class of long noncoding RNAs (lncRNAs) are dysregulated in hepatocellular carcinoma (HCC) and they are closely related with tumorigenesis. Our previous studies indicated that LINC00052 was a downregulated lncRNA in HCC and acted as a tumor suppressor gene. Using transcription microarray analysis, we found that knockdown of LINC00052 resulted in EPB41L3 downregulation. However, the function of EPB41L3 and the mechanism of LINC00052 downregulating EPB41L3 in HCC remain unclear. In this study, we found that overexpression of LINC00052 could upregulate the EPB41L3 expression and it might serve as a tumor suppressor gene in HCC. Database analysis showed that miR-452-5P could target LINC00052. The binding regions between LINC00052 and miR-452-5P were confirmed by luciferase assays. Moreover, LINC00052 inhibited cell malignant behavior by increasing miR-452-5P expression, suggesting that LINC00052 was negatively regulated by miR-452-5P. In addition, overexpression of miR-452-5P resulted in a decrease of EPB41L3 expression, suggesting that EPB41L3 was as a target of miR-452-5P. In conclusion, these results demonstrated that a novel pathway was mediated by LINC00052 in HCC.