m6A Writer METTL3-Mediated lncRNA LINC01125 Prevents the Malignancy of Papillary Thyroid Cancer.

IF 0.8 4区医学 Q4 IMMUNOLOGY

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI:10.1615/CritRevImmunol.2023050267

Tianyou He, Hailiang Xia, Baojie Chen, Ziqi Duan, Chaogang Huang

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引用次数: 0

Abstract

Background: Long non-coding RNA (lncRNA) LINC01125 is an anti-tumor factor in a variety of tumors, and regulates cancer cell function. However, its function and mechanism of N6-methyladenosine (m6A) modification in papillary thyroid cancer (PTC) tumorigenesis remain unclear.

Aims: This study aimed to reveal the function and m6A modification of LINC01125 in PTC tumorigenesis.

Methods: The LINC01125 and methyltransferase-like 3 (METTL3) levels in PTC cells and tissues was assessed by qRT-PCR. The binding relationship among LINC01125 and METTL3 was determined by MeRIP, Pearson, bioinformatics, and RNA stabilization analysis. Transwell assays were performed to confirm the changes of PTC cell migration and invasion. Cell proliferation was revealed by CCK-8 as well as colony formation assays.

Results: Low expression of LINC01125 and METTL3 was identified in PTC. LINC01125 was a downstream target of METTL3-mediated m6A modification and was stably upregulated via METTL3. Cell invasion, migration, viability, and colony formation levels were decreased when LINC01125 or METTL3 was upregulated. Inhibition of LINC01125 had the opposite impact, promoting cell proliferation and metastasis, and reversing METTL3 overexpression-resulted cell malignancy suppression.

Conclusions: Overall, this study proved that the m6A modification of LINC01125 was mediated by METTL3 and LINC01125 inhibited cell invasion, migration and proliferation, thereby suppressing the development of PTC. This points to the LINC01125-m6A-METTL3 axis as a possible prospective target for future treatment of PTC.

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m6A书写器METTL3-介导的lncRNA LINC01125预防癌症乳头状甲状腺的恶性肿瘤。

背景：长非编码RNA（lncRNA）LINC01125是多种肿瘤的抗肿瘤因子，调节癌症细胞功能。然而，其N6-甲基腺苷（m6A）修饰在甲状腺乳头状癌症（PTC）肿瘤发生中的作用和机制尚不清楚。目的：本研究旨在揭示LINC01125在PTC肿瘤发生中的作用和m6A修饰。方法：采用qRT-PCR检测PTC细胞和组织中LINC01125和甲基转移酶样3（METTL3）的水平。通过MeRIP、Pearson、生物信息学和RNA稳定分析确定LINC01125和METTL3之间的结合关系。进行Transwell测定以确认PTC细胞迁移和侵袭的变化。通过CCK-8以及集落形成测定来揭示细胞增殖。结果：在PTC中发现LINC01125和METTL3的低表达。LINC01125是METTL3介导的m6A修饰的下游靶标，并通过METTL3稳定上调。当LINC01125或METTL3上调时，细胞侵袭、迁移、活力和集落形成水平降低。LINC01125的抑制具有相反的影响，促进细胞增殖和转移，逆转METTL3过表达导致细胞恶性肿瘤抑制。结论：总之，本研究证明了LINC01125的m6A修饰是由METTL3介导的，LINC0112五抑制了细胞的侵袭、迁移和增殖，从而抑制了PTC的发展。这表明LINC01125-m6A-METTL3轴可能是未来PTC治疗的前瞻性靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Critical Reviews in Immunology 医学-免疫学

CiteScore

2.60

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Immunology covers a broad spectrum of investigations at the genes, molecular, cellular, organ and system levels to reveal defense mechanisms against pathogens as well as protection against tumors and autoimmune diseases. The great advances in immunology in recent years make this field one of the most dynamic and rapidly growing in medical sciences. Critical ReviewsTM in Immunology (CRI) seeks to present a balanced overview of contemporary adaptive and innate immune responses related to autoimmunity, tumor, microbe, transplantation, neuroimmunology, immune regulation and immunotherapy from basic to translational aspects in health and disease. The articles that appear in CRI are mostly obtained by invitations to active investigators. But the journal will also consider proposals from the scientific community. Interested investigators should send their inquiries to the editor before submitting a manuscript.