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m6A修饰在内分泌癌中的新兴作用

The Emerging Role of m6A Modification in Endocrine Cancer.

作者信息

Ji Xiaoyu, Wang Zhiyuan, Sun Wei, Zhang Hao

机构信息

Department of Thyroid Surgery, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang 110001, China.

出版信息

Cancers (Basel). 2023 Feb 6;15(4):1033. doi: 10.3390/cancers15041033.

DOI:10.3390/cancers15041033
PMID:36831377
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9954123/
Abstract

With the development of RNA modification research, N6-methyladenosine (m6A) is regarded as one of the most important internal epigenetic modifications of eukaryotic mRNA. It is also regulated by methylase, demethylase, and protein preferentially recognizing the m6A modification. This dynamic and reversible post-transcriptional RNA alteration has steadily become the focus of cancer research. It can increase tumor stem cell self-renewal and cell proliferation. The m6A-modified genes may be the primary focus for cancer breakthroughs. Although some endocrine cancers are rare, they may have a high mortality rate. As a result, it is critical to recognize the significance of endocrine cancers and identify new therapeutic targets that will aid in improving disease treatment and prognosis. We summarized the latest experimental progress in the m6A modification in endocrine cancers and proposed the m6A alteration as a potential diagnostic marker for endocrine malignancies.

摘要

随着RNA修饰研究的发展,N6-甲基腺苷(m6A)被视为真核生物mRNA最重要的内部表观遗传修饰之一。它还受到甲基化酶、去甲基化酶以及优先识别m6A修饰的蛋白质的调控。这种动态可逆的转录后RNA改变已逐渐成为癌症研究的焦点。它可以增加肿瘤干细胞的自我更新和细胞增殖。m6A修饰的基因可能是癌症突破的主要关注点。尽管一些内分泌癌很少见,但它们可能具有较高的死亡率。因此,认识到内分泌癌的重要性并确定有助于改善疾病治疗和预后的新治疗靶点至关重要。我们总结了内分泌癌中m6A修饰的最新实验进展,并提出m6A改变作为内分泌恶性肿瘤的潜在诊断标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/9954123/08a60d5aaf25/cancers-15-01033-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/9954123/aee3512b2a84/cancers-15-01033-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/9954123/08a60d5aaf25/cancers-15-01033-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/9954123/aee3512b2a84/cancers-15-01033-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/9954123/08a60d5aaf25/cancers-15-01033-g002.jpg

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N(6)-methyladenosine methylation-regulated polo-like kinase 1 cell cycle homeostasis as a potential target of radiotherapy in pancreatic adenocarcinoma.N(6)-甲基腺苷甲基化调控的类 polo 样激酶 1 细胞周期平衡作为胰腺腺癌放疗的潜在靶点。
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HIF-1 Regulated WTAP Overexpression Promoting the Warburg Effect of Ovarian Cancer by m6A-Dependent Manner.HIF-1 调控 WTAP 过表达通过 m6A 依赖的方式促进卵巢癌细胞的瓦博格效应。
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FTO Prevents Thyroid Cancer Progression by SLC7A11 m6A Methylation in a Ferroptosis-Dependent Manner.
FTO通过SLC7A11的m6A甲基化以铁死亡依赖的方式抑制甲状腺癌进展。
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LncRNA-PACERR induces pro-tumour macrophages via interacting with miR-671-3p and m6A-reader IGF2BP2 in pancreatic ductal adenocarcinoma.长链非编码 RNA-PACERR 通过与 miR-671-3p 和 m6A 阅读器 IGF2BP2 相互作用诱导胰腺导管腺癌中的促肿瘤巨噬细胞。
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METTL3-mediated m6A modification of STEAP2 mRNA inhibits papillary thyroid cancer progress by blocking the Hedgehog signaling pathway and epithelial-to-mesenchymal transition.METTL3 介导的 STEAP2 mRNA m6A 修饰通过阻断 Hedgehog 信号通路和上皮间质转化抑制甲状腺乳头状癌的进展。
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RNA N6-methyladenosine demethylase FTO promotes pancreatic cancer progression by inducing the autocrine activity of PDGFC in an mA-YTHDF2-dependent manner.RNA N6-甲基腺嘌呤去甲基酶 FTO 通过诱导 mA-YTHDF2 依赖性 PDGFC 的自分泌活性促进胰腺癌进展。
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mA RNA demethylase FTO promotes the growth, migration and invasion of pancreatic cancer cells through inhibiting TFPI-2.mA RNA 去甲基酶 FTO 通过抑制 TFPI-2 促进胰腺癌细胞的生长、迁移和侵袭。
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Targeting IGF2BP2 Promotes Differentiation of Radioiodine Refractory Papillary Thyroid Cancer via Destabilizing RUNX2 mRNA.靶向IGF2BP2通过使RUNX2 mRNA不稳定促进放射性碘难治性乳头状甲状腺癌的分化。
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