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长链非编码 RNA ROR 通过与 miR-223-3p 相互作用抑制肿瘤抑制基因 NF2 促进结直肠癌的增殖和侵袭。

Long noncoding RNA ROR promotes proliferation and invasion of colorectal cancer by inhibiting tumor suppressor gene NF2 through interacting with miR-223-3p.

机构信息

Department of Education and Science, Affiliated Hospital of Weifang Medical University, Weifang City, Shandong Province, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Mar;24(5):2401-2411. doi: 10.26355/eurrev_202003_20507.

DOI:10.26355/eurrev_202003_20507
PMID:32196591
Abstract

OBJECTIVE

Colorectal cancer is one of the most common cancers in the world. LncRNA ROR, is a tumor oncogene associated with various human cancers. However, the role of ROR in colorectal cancer cells still remains unknown. The aim of this study was to measure the expression level of ROR and clarify its biological functions in colorectal cancer cells.

MATERIALS AND METHODS

The expression level of ROR in colorectal cancer cells was detected using qRT-PCR. We performed CCK8 assay, colony formation assay, cell migration and invasion assays to evaluate the effects of ROR on cell proliferation, migration and invasion of colorectal cancer cells. Then, transfection of ROR, ROR inhibitor, miRNA-223-3p-mimics and miRNA-223-3p-inhibitor, qRT-PCR, and luciferase reporter assay were used to explore the molecular mechanisms.

RESULTS

In the present study, Lnc-ROR was highly expressed in colorectal cancers compared with adjacent non-cancerous normal tissues. And the expression level of ROR was also increased in colorectal cancer cells (p < 0.05). CCK8 assay and invasion assay suggested that ROR can promote cell proliferation and invasion. The luciferase reporter assay showed ROR acted as sponge and directly competed with miRNA-223-3p, then decreasing the expression of tumor suppressor gene NF2.

CONCLUSIONS

The findings of this study first revealed that ROR was upregulated in colorectal cancer cells and can promote cell proliferation and invasion by inhibiting tumor suppressor gene NF2 through interacting with miR-223-3p.

摘要

目的

结直肠癌是世界上最常见的癌症之一。LncRNA ROR 是与多种人类癌症相关的肿瘤癌基因。然而,ROR 在结直肠癌细胞中的作用尚不清楚。本研究旨在测量 ROR 的表达水平,并阐明其在结直肠癌细胞中的生物学功能。

材料和方法

使用 qRT-PCR 检测结直肠癌细胞中 ROR 的表达水平。我们进行了 CCK8 测定、集落形成测定、细胞迁移和侵袭测定,以评估 ROR 对结直肠癌细胞增殖、迁移和侵袭的影响。然后,通过转染 ROR、ROR 抑制剂、miRNA-223-3p 模拟物和 miRNA-223-3p 抑制剂、qRT-PCR 和荧光素酶报告基因测定来探索分子机制。

结果

在本研究中,与相邻的非癌性正常组织相比,Lnc-ROR 在结直肠癌中高度表达。并且结直肠癌细胞中 ROR 的表达水平也增加(p<0.05)。CCK8 测定和侵袭测定表明 ROR 可以促进细胞增殖和侵袭。荧光素酶报告基因测定显示 ROR 作为海绵直接与 miRNA-223-3p 竞争,从而降低肿瘤抑制基因 NF2 的表达。

结论

本研究的结果首次表明,ROR 在结直肠癌细胞中上调,并通过与 miR-223-3p 相互作用抑制肿瘤抑制基因 NF2,从而促进细胞增殖和侵袭。

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