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MEG3抑制人骨肉瘤细胞的增殖和侵袭并促进其凋亡。

MEG3 inhibits proliferation and invasion and promotes apoptosis of human osteosarcoma cells.

作者信息

Shi Yao, Lv Chen, Shi Li, Tu Guanjun

机构信息

Department of Orthopaedic Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Department of Orthopaedic Surgery, The First Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.

出版信息

Oncol Lett. 2018 Feb;15(2):1917-1923. doi: 10.3892/ol.2017.7463. Epub 2017 Nov 21.

Abstract

Osteosarcoma is known as a malignant tumour with a high mortality rate in orthopaedic settings; however, the factors associated with its degree of malignancy and the biological response remains to be elucidated. Although the essential role of the long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) has been recently reported, its biological functions and regulatory mechanism in osteosarcoma cells have not yet been reported. In the present study, reverse transcription-quantitative polymerase chain reaction analysis revealed that the expression of MEG3 in MG63 cells was lower compared with in hFOB1.19 cells. Furthermore, it was observed that overexpressing MEG3 in MG63 cells resulted in a decline in the proliferation and invasion, and a marked increase in apoptosis. Additionally, western blotting was used to detect the changes in expression of p53 and MDM2 proto-oncogene, which may be regulated by MEG3, and proteins that associated with cell proliferation, invasion and apoptosis. It was demonstrated that the upregulation of MEG3 significantly increased the transactivation of p53 and induced downstream changes in protein expression. In conclusion, these experiments have demonstrated that MEG3 serves an essential regulatory role in the biological processes of human osteosarcoma cells, and imply that MEG3 may be a marker for predicting the occurrence and development of osteosarcoma.

摘要

骨肉瘤是骨科领域中一种死亡率很高的恶性肿瘤;然而,与其恶性程度和生物学反应相关的因素仍有待阐明。尽管最近报道了长链非编码RNA(lncRNA)母系表达基因3(MEG3)的重要作用,但其在骨肉瘤细胞中的生物学功能和调控机制尚未见报道。在本研究中,逆转录-定量聚合酶链反应分析显示,与hFOB1.19细胞相比,MG63细胞中MEG3的表达较低。此外,观察到在MG63细胞中过表达MEG3会导致增殖和侵袭能力下降,凋亡显著增加。此外,采用蛋白质印迹法检测可能受MEG3调控的p53和MDM2原癌基因的表达变化,以及与细胞增殖、侵袭和凋亡相关的蛋白质。结果表明,MEG3的上调显著增加了p53的反式激活,并诱导了下游蛋白质表达的变化。总之,这些实验表明MEG3在人骨肉瘤细胞的生物学过程中起重要调控作用,并提示MEG3可能是预测骨肉瘤发生发展的一个标志物。

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