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通过负向调节 上调 来促进MG63细胞的增殖、迁移和侵袭。

promotes proliferation, migration, and invasion of MG63 cells by upregulation of via negatively regulating .

作者信息

Liu Kai, Zhang Yingang, Liu Liang, Yuan Qiling

机构信息

Department of Orthopedics, The First Affliated Hospital of Xi'an Jiaotong University, Xi'an, China,

出版信息

Onco Targets Ther. 2018 Dec 4;11:8729-8740. doi: 10.2147/OTT.S182993. eCollection 2018.

Abstract

PURPOSE

This article aimed to investigate the mechanism by which and affected the development of osteosarcoma.

METHODS

Tumor tissues and adjacent tissues of 23 osteosarcoma patients were collected. Normal osteoblasts hFOB1.19 and osteosarcoma cells MG63 were cultured. MG63 cells were transfected and grouped: si-negative control (NC) group, si-MALAT1 group, miR-129 NC group, miR-129 mimics group, p-Empty vector group, p-MALAT1 group, p-MALAT1+ miR-129 mimics group, and p-MALAT1+ si-TGIF2 group. Luciferase reporter assay, Cell Counting Kit-8 assay, Transwell assay, quantitative reverse transcription PCR, Western blot, and Pearson correlation analysis were performed.

RESULTS

expression in tumor tissues and MG63 cells was increased (<0.01). High expression predicted poor prognosis of osteosarcoma patients. MG63 cells of si-MALAT1 group exhibited much lower cell viability, migration, and invasive cell numbers when compared with si-NC group (<0.01). For MG63 cells of miR-129 mimics group, they had markedly lower cell viability, migration, and invasive cell numbers than miR-129 NC group (<0.01). was targetedly and negatively regulated by . , which was targetedly and negatively regulated by , was overexpressed in tumor tissues and MG63 cells (<0.01). overexpresison and downregulation significantly reversed the enhanced cell viability, migration, and invasion induced by (<0.01).

CONCLUSION

promotes expression through negative regulation of , which further promotes the proliferation, migration, and invasion of MG63 cells.

摘要

目的

本文旨在研究[具体物质1]和[具体物质2]影响骨肉瘤发展的机制。

方法

收集23例骨肉瘤患者的肿瘤组织及相邻组织。培养正常成骨细胞hFOB1.19和骨肉瘤细胞MG63。对MG63细胞进行转染并分组:小干扰RNA阴性对照组(si-NC组)、小干扰RNA-MALAT1组、miR-129阴性对照组、miR-129模拟物组、空载体组、MALAT1组、MALAT1+miR-129模拟物组以及MALAT1+小干扰RNA-TGIF2组。进行荧光素酶报告基因检测、细胞计数试剂盒-8检测、Transwell检测、定量逆转录聚合酶链反应、蛋白质印迹法以及Pearson相关性分析。

结果

[具体物质1]在肿瘤组织和MG63细胞中的表达增加(P<0.01)。[具体物质1]高表达预示骨肉瘤患者预后不良。与si-NC组相比,si-MALAT1组的MG63细胞表现出更低的细胞活力、迁移能力和侵袭细胞数量(P<0.01)。对于miR-129模拟物组的MG63细胞,其细胞活力、迁移能力和侵袭细胞数量明显低于miR-129阴性对照组(P<0.01)。[具体物质1]受到[具体物质2]的靶向负调控。[具体物质3]受到[具体物质2]的靶向负调控,在肿瘤组织和MG63细胞中过表达(P<0.01)。[具体物质1]过表达和[具体物质2]下调显著逆转了由[具体物质3]诱导的增强的细胞活力、迁移和侵袭(P<0.01)。

结论

[具体物质1]通过对[具体物质2]的负调控促进[具体物质3]表达,进而促进MG63细胞的增殖、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcf1/6287664/ea001c7eea77/ott-11-8729Fig1.jpg

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