靶向miR-205-5p的长链非编码RNA转移相关肺腺癌转录因子1参与鼻咽癌细胞生长

Yuetang Mi, Haiyan Li, Jingchuan He
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引用次数: 0

摘要

鼻咽癌(NC)的发病率呈上升趋势。NC的预后仍不理想;因此,有必要寻找新的方法来改善它。LncRNA MALAT1 (MALAT1)是一个被广泛研究的基因,但其在NC中的地位尚不清楚。需要更多的实验分析来揭示MALAT1在NC中的作用,为NC的诊断和治疗提供可靠和准确的理论依据。首先,将2018年2月至2020年3月在我院住院的NC患者和同期体检的健康对照纳入本研究。检测患者外周血和组织中的MALAT1和miR-205-5p。在NC患者中,MALAT1高表达,miR-205-5p低表达。两种基因均能有效预测NC的发生,且表达呈负相关。体外实验表明,抑制MALAT1、升高miR-205-5p可降低CNE-2Z细胞的增殖,提高其凋亡率。然而,增加MALAT1和抑制miR-205-5p具有相反的作用。通过在线网站ENCORI,在MALAT1和miR-205-5p中发现了互补位点。根据双荧光素酶报告基因检测,共转染miR-205-5p-min可抑制MALAT1-WT的荧光素酶活性,而共转染miR-205-5p-inh可增强MALAT1-MUT的荧光素酶活性。最后,通过救援实验,我们发现MALAT1 si-RNA+miR-205-5p-inh组和MALAT1+NC-RNA组细胞的生物学行为没有差异。因此,MALAT1通过特异性调节miR-205-5p促进NC细胞增殖,抑制凋亡,参与NC的发育。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long-Chain Non-Coding RNAs Metastasis-Associated Lung Adenocarcinoma Transcript-1 Is Involved in Growth of Nasopharyngeal Carcinoma Cells by Targeting miR-205-5p
The incidence of nasopharyngeal carcinoma (NC) has been rising. The prognosis of NC remains unsatisfactory; therefore, it is necessary to find new ways to improve it. LncRNA MALAT1 (MALAT1) is a well-studied gene, but its status in NC remains unclear. More experimental analyses are needed to uncover the role of MALAT1 in NC for a reliable and accurate theoretical basis for NC’s diagnosis and treatment. First, NC patients admitted to our hospital from February 2018 to March 2020 and healthy controls who underwent physical examinations during the same period were enrolled in this study. MALAT1 and miR-205-5p in the patients’ peripheral blood and tissues were detected. The expression of MALAT1 was high, and the expression of miR-205-5p was low in the NC patients. Both genes were effective in predicting the occurrence of NC, and their expression was negatively correlated. According to in vitro experiments, inhibiting MALAT1 and increasing miR-205-5p could reduce CNE-2Z cells’ proliferation and increase their apoptotic rate. However, increasing MALAT1 and inhibiting miR-205-5p had opposite effects. Through the online website ENCORI, complementary sites were found in MALAT1 and miR-205-5p. According to dual-luciferase reporter gene assay, MALAT1-WT’s luciferase activity was inhibited by the co-transfection of miR-205-5p-min, while MALAT1-MUT’s luciferase activity was enhanced by the co-transfection of miR-205-5p-inh. Lastly, through rescue experiments, we found no difference in the biological behavior between the cells in the MALAT1 si-RNA+miR-205-5p-inh group and the MALAT1+NC-RNA group. Therefore, MALAT1 promotes NC cell proliferation, inhibits apoptosis, and participates in NC’s development via specifically regulating miR-205-5p.
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来源期刊
Nanoscience and Nanotechnology Letters
Nanoscience and Nanotechnology Letters Physical, Chemical & Earth Sciences-MATERIALS SCIENCE, MULTIDISCIPLINARY
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