Long non‑coding RNA XIST serves an oncogenic role in osteosarcoma by sponging miR‑137

Li,Hui; Cui,Jingjing; Xu,Bin; He,Shuguang; Yang,Haiyan; Liu,Lingzhi

doi:10.3892/etm.2018.7032

Long non‑coding RNA XIST serves an oncogenic role in osteosarcoma by sponging miR‑137

Authors:
- Hui Li
- Jingjing Cui
- Bin Xu
- Shuguang He
- Haiyan Yang
- Lingzhi Liu
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Affiliations: Department of Microbiology and Immunology, Medical School of Jishou University, Jishou, Hunan 416000, P.R. China, Department of Medical Insurance, Affiliated Hospital of Binzhou Medical School, Binzhou, Shandong 256603, P.R. China, Research Center of Translational Medicine, School of Medicine, Da Tian Wan Campus of Jishou University, Jishou, Hunan 416000, P.R. China, Clinical Laboratory, First Affiliated Hospital of Hunan College of Traditional Chinese Medicine, Zhuzhou, Hunan 412000, P.R. China, Department of Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530000, P.R. China
Published online on: November 29, 2018 https://doi.org/10.3892/etm.2018.7032
Pages: 730-738
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The long non‑coding RNA X inactive‑specific transcript (XIST) has been implicated in certain human cancers, including osteosarcoma (OS), but the molecular mechanism of XIST underlying OS progression remains to be fully uncovered. In the present study, reverse transcription‑quantitative polymerase chain reaction data demonstrated that XIST was significantly upregulated in OS tissues and cell lines (Saos‑2, U2OS, HOS and MG63) compared with adjacent non‑tumour tissues and normal human osteoblast cell line HFOB1.19. Bioinformatics analysis and luciferase reporter gene assay data demonstrated that XIST could directly target microRNA (miR)‑137 and negatively regulate the expression of miR‑137 in Saos‑2 and U2OS cells. Furthermore, miR‑137 was markedly downregulated in OS tissues and cell lines. An inverse association between XIST and miR‑137 expression was observed in OS tissues. Knockdown of XIST caused a significant reduction in cell proliferation and invasion and suppressed matrix metalloproteinase (MMP2) and MMP9 protein levels in Saos‑2 and U2OS cells. Furthermore, inhibition of miR‑137 expression abolished the effects of XIST downregulation on the proliferation and invasion of OS cells. In summary, the present study suggests that XIST promotes OS cell proliferation and invasion by inhibition of miR‑137 expression. Thus, XIST may be a potential therapeutic target for the treatment of OS.

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