Research Papers:

MALAT1 promotes osteosarcoma development by targeting TGFA via MIR376A

Wei Luo, Hongbo He, Wenfeng Xiao, Qing Liu, Zhenhan Deng, Yaojuan Lu, Qian Wang, Qiping Zheng and Yusheng Li _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:54733-54743. https://doi.org/10.18632/oncotarget.10752

Metrics: PDF 2585 views  |   HTML 3189 views  |   ?  


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

Correspondence to:

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.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 10752