LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma

// Haibing Xiao 1, 2 , Kun Tang 1, 2 , Peijun Liu 1, 2 , Ke Chen 1, 2 , Junhui Hu 1, 2 , Jin Zeng 1, 2 , Wei Xiao 3 , Gan Yu 1, 2 , Weiming Yao 1, 2 , Hui Zhou 1, 2 , Heng Li 1, 2 , Yingtian Pan 4 , Anping Li 5 , Zhangqun Ye 1, 2 , Ji Wang 6 , Hua Xu 1, 2 , Qihong Huang 5 1 Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 2 Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 3 Translational Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 4 Department of Biomedical Engineering, Stony Brook University, Stony Brook, New York 11794, USA 5 The Wistar Institute, Philadelphia, Pennsylvania 19104, USA 6 Department of Cell Death and Cancer Genetics, The Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA Correspondence to: Hua Xu, e-mail: xuhua@mail.hust.edu.cn Ji Wang, e-mail: jiwang924@gmail.com Keywords: lncRNA, MALAT1, miR-200s, ZEB2, KIRC Received: April 22, 2015      Accepted: September 25, 2015      Published: October 09, 2015 ABSTRACT Long non-coding RNA (lncRNAs) play a critical role in the development of cancers. LncRNA metastasis-associated lung adenocarcinoma transcript 1(MALAT1) has recently been identified to be involved in tumorigenesis of several cancers such as lung cancer, bladder cancer and so on. Here, we found that MALAT1 exist a higher fold change (Tumor/Normal) in clear cell kidney carcinoma (KIRC) from The Cancer Genome Atlas (TCGA) Data Portal and a negative correlation with miR-200s family. We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo . In addition, miR-200c can partly reverse the MALAT1′s stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC. The inhibition of MALAT1 expression may be a promising strategy for KIRC therapy.