LncRNA MIR600HG inhibits laryngeal cancer development by mediating the miR-424-5p/BTG2 axis

IF 4.5 2区 医学 Q1 ONCOLOGY Cancer Science Pub Date : 2024-12-01 DOI:10.1111/cas.16404
Xiaowen Zhu, Min Zhong, Qingdong Wang, MeiJia Zhang
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Abstract

Laryngeal carcinoma is the predominant kind of tumor seen under the category of head and neck malignancies. LncRNA MIR600HG affects tumor morphology in numerous cancer types. However, the function of MIR600HG in laryngeal cancer remains unclear. Protein and gene expressions were analyzed by using western blot and quantitative real time polymerase chain reaction. Cells proliferation and migration were evaluated by EdU and transwell assays. Flow cytometry was performed to detect cells apoptosis. The interaction between MIR600HG or B-cell translocation gene 2 (BTG2) and miR-424-5p was analyzed by dual luciferase reporter assay and RNA immunoprecipitation. The expression of MIR600HG in laryngeal cancer tissues was lower than that in normal tissues, and low expression of MIR600HG was associated with poor prognosis in laryngeal cancer. Furthermore, overexpression of MIR600HG resulted in a reduction in cellular proliferation and the promotion of apoptosis in both HEp-2 and Tu-212. Mechanically, miR-424-5p was a direct target of MIR600HG, and overexpression of MIR600HG reduced miR-424-5p expression. Furthermore, BTG2 was a target gene of miR-424-5p and miR-424-5p upregulation suppressed the expression of BTG2. In addition, overexpression of BTG2 inhibited laryngeal cancer progression, whereas MIR600HG knockdown or miR-424-5p overexpression reversed the role of BTG2. This work suggested that MIR600HG represses laryngeal tumor development by regulating the miR-424-5p/BTG2 axis, which provides new molecules for early diagnosis of laryngeal cancer in the future.

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LncRNA MIR600HG通过介导miR-424-5p/BTG2轴抑制喉癌的发展。
喉癌是头颈部恶性肿瘤的主要类型。LncRNA MIR600HG影响多种癌症类型的肿瘤形态。然而,MIR600HG在喉癌中的作用尚不清楚。采用western blot和定量实时聚合酶链反应分析蛋白和基因表达。用EdU和transwell检测细胞增殖和迁移情况。流式细胞术检测细胞凋亡情况。采用双荧光素酶报告基因法和RNA免疫沉淀法分析MIR600HG或b细胞易位基因2 (BTG2)与miR-424-5p的相互作用。MIR600HG在喉癌组织中的表达低于正常组织,MIR600HG的低表达与喉癌预后不良相关。此外,MIR600HG的过表达导致HEp-2和Tu-212细胞增殖减少,细胞凋亡促进。机械上,miR-424-5p是MIR600HG的直接靶点,MIR600HG过表达会降低miR-424-5p的表达。此外,BTG2是miR-424-5p的靶基因,miR-424-5p上调可抑制BTG2的表达。此外,BTG2的过表达抑制了喉癌的进展,而MIR600HG的下调或miR-424-5p的过表达逆转了BTG2的作用。本研究提示MIR600HG通过调控miR-424-5p/BTG2轴抑制喉部肿瘤的发展,为今后喉癌的早期诊断提供了新的分子。
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来源期刊
Cancer Science
Cancer Science 医学-肿瘤学
自引率
3.50%
发文量
406
审稿时长
2 months
期刊介绍: Cancer Science (formerly Japanese Journal of Cancer Research) is a monthly publication of the Japanese Cancer Association. First published in 1907, the Journal continues to publish original articles, editorials, and letters to the editor, describing original research in the fields of basic, translational and clinical cancer research. The Journal also accepts reports and case reports. Cancer Science aims to present highly significant and timely findings that have a significant clinical impact on oncologists or that may alter the disease concept of a tumor. The Journal will not publish case reports that describe a rare tumor or condition without new findings to be added to previous reports; combination of different tumors without new suggestive findings for oncological research; remarkable effect of already known treatments without suggestive data to explain the exceptional result. Review articles may also be published.
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