LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma
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Haibing Xiao1,2, Kun Tang1,2, Peijun Liu1,2, Ke Chen1,2, Junhui Hu1,2, Jin Zeng1,2, Wei Xiao3, Gan Yu1,2, Weiming Yao1,2, Hui Zhou1,2, Heng Li1,2, Yingtian Pan4, Anping Li5, Zhangqun Ye1,2, Ji Wang6, Hua Xu1,2, Qihong Huang5
1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
2Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
3Translational Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
4Department of Biomedical Engineering, Stony Brook University, Stony Brook, New York 11794, USA
5The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
6Department of Cell Death and Cancer Genetics, The Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA
Hua Xu, e-mail: [email protected]
Ji Wang, e-mail: [email protected]
Keywords: lncRNA, MALAT1, miR-200s, ZEB2, KIRC
Received: April 22, 2015 Accepted: September 25, 2015 Published: October 09, 2015
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.
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