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环氧合酶-2过表达的人骨肉瘤细胞系中的基因表达分析

Analysis of gene expression in cyclooxygenase-2-overexpressed human osteosarcoma cell lines.

作者信息

Han Jeong A, Kim Ji-Yeon, Kim Jong-Il

机构信息

Department of Biochemistry and Molecular Biology, Kangwon National University School of Medicine, Chuncheon 200-701, Korea.

Department of Internal Medicine, Seoul National University Hospital, Seoul 110-744, Korea.

出版信息

Genomics Inform. 2014 Dec;12(4):247-53. doi: 10.5808/GI.2014.12.4.247. Epub 2014 Dec 31.

DOI:10.5808/GI.2014.12.4.247
PMID:25705166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4330262/
Abstract

Osteosarcoma is the most common primary bone tumor, generally affecting young people. While the etiology of osteosarcoma has been largely unknown, recent studies have suggested that cyclooxygenase-2 (COX-2) plays a critical role in the proliferation, migration, and invasion of osteosarcoma cells. To understand the mechanism of action of COX-2 in the pathogenesis of osteosarcoma, we compared gene expression patterns between three stable COX-2-overexpressing cell lines and three control cell lines derived from U2OS human osteosarcoma cells. The data showed that 56 genes were upregulated, whereas 20 genes were downregulated, in COX-2-overexpressed cell lines, with an average fold-change > 1.5. Among the upregulated genes, COL1A1, COL5A2, FBN1, HOXD10, RUNX2, and TRAPPC2are involved in bone and skeletal system development, while DDR2, RAC2, RUNX2, and TSPAN31are involved in the positive regulation of cell proliferation. Among the downregulated genes, HIST1H1D, HIST1H2AI, HIST1H3H, and HIST1H4C are involved in nucleosome assembly and DNA packaging. These results may provide useful information to elucidate the molecular mechanism of the COX-2-mediated malignant phenotype in osteosarcoma.

摘要

骨肉瘤是最常见的原发性骨肿瘤,通常影响年轻人。虽然骨肉瘤的病因在很大程度上尚不清楚,但最近的研究表明,环氧合酶-2(COX-2)在骨肉瘤细胞的增殖、迁移和侵袭中起关键作用。为了了解COX-2在骨肉瘤发病机制中的作用机制,我们比较了三种稳定过表达COX-2的细胞系与三种源自U2OS人骨肉瘤细胞的对照细胞系之间的基因表达模式。数据显示,在COX-2过表达的细胞系中,有56个基因上调,20个基因下调,平均变化倍数>1.5。在上调的基因中,COL1A1、COL5A2、FBN1、HOXD10、RUNX2和TRAPPC2参与骨骼系统发育,而DDR2、RAC2、RUNX2和TSPAN31参与细胞增殖的正调控。在下调的基因中,HIST1H1D、HIST1H2AI、HIST1H3H和HIST1H4C参与核小体组装和DNA包装。这些结果可能为阐明COX-2介导的骨肉瘤恶性表型的分子机制提供有用信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acef/4330262/900e4cbf50f0/gni-12-247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acef/4330262/eeeabac2e838/gni-12-247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acef/4330262/900e4cbf50f0/gni-12-247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acef/4330262/eeeabac2e838/gni-12-247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acef/4330262/900e4cbf50f0/gni-12-247-g002.jpg

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