MALAT1 promotes osteosarcoma development by targeting TGFA via MIR376A
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Wei Luo1, Hongbo He1, Wenfeng Xiao1, Qing Liu1, Zhenhan Deng1, Yaojuan Lu2, Qian Wang2, Qiping Zheng2, Yusheng Li1
1Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008, China
2Department of Hematological Laboratory Science, Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang 212013, China
Yusheng Li, email: [email protected]
Qiping Zheng, email: [email protected]
Keywords: IncRNA, MALAT1, MIR376A, osteosarcoma, TGFA
Received: May 25, 2016 Accepted: July 08, 2016 Published: July 21, 2016
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA) that contributes to the initiation and development of many solid tumors, including osteosarcoma (OS). Here, we showed that MALAT1 was increased in human OS cell lines and tissues and promoted OS cell growth, while MALAT1 knockdown suppressed OS cell growth. We also detected downregulation of MIR376A, a suppressor of OS growth, and upregulation of TGFA, a promoter of OS growth, in OS tissues. TGFA expression was positively correlated with MALAT1 expression, and both were negatively correlated with MIR376A expression. There was a direct interaction between MIR376A and MALAT1 via a putative MIR376A binding site within the MALAT1 3’-untranslated region (3’-UTR). There was also a direct interaction between MIR376A and the TGFA 3’-UTR. Thus, MALAT1 may promote OS cell growth through inhibition of MIR376A, leading to increased expression of TGFA. Our results suggest a MALAT1/MIR376A/TGFA axis mediates OS cell proliferation and tumor progression.
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