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前列腺癌中 mA 甲基化的研究进展。

Research progress of mA methylation in prostate cancer.

机构信息

Department of Urology, The Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang 110042, China.

出版信息

Asian J Androl. 2023 Mar-Apr;25(2):166-170. doi: 10.4103/aja202265.

DOI:10.4103/aja202265
PMID:36308073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10069701/
Abstract

N-methyladenosine (mA) is a ubiquitous RNA modification in mammals. This modification is "written" by methyltransferases and then "read" by mA-binding proteins, followed by a series of regulation, such as alternative splicing, translation, RNA stability, and RNA translocation. At last, the modification is "erased" by demethylases. mA modification is essential for normal physiological processes in mammals and is also a very important epigenetic modification in the development of cancer. In recent years, cancer-related mA regulation has been widely studied, and various mechanisms of mA regulation in cancer have also been recognized. In this review, we summarize the changes of mA modification in prostate cancer and discuss the effect of mA regulation on prostate cancer progression, aiming to profile the potential relevance between mA regulation and prostate cancer development. Intensive studies on mA regulation in prostate cancer may uncover the potential role of mA methylation in the cancer diagnosis and cancer therapy.

摘要

N6-甲基腺苷(m6A)是哺乳动物中普遍存在的一种 RNA 修饰。这种修饰由甲基转移酶“书写”,然后由 m6A 结合蛋白“读取”,随后进行一系列的调控,如可变剪接、翻译、RNA 稳定性和 RNA 易位。最后,修饰由去甲基酶“擦除”。m6A 修饰对于哺乳动物的正常生理过程至关重要,也是癌症发生过程中非常重要的一种表观遗传修饰。近年来,与癌症相关的 m6A 调控受到了广泛研究,并且已经认识到了 m6A 调控在癌症发展过程中的各种机制。在这篇综述中,我们总结了前列腺癌中 m6A 修饰的变化,并讨论了 m6A 调控对前列腺癌进展的影响,旨在探讨 m6A 调控与前列腺癌发展之间的潜在相关性。对前列腺癌中 m6A 调控的深入研究可能揭示 m6A 甲基化在癌症诊断和癌症治疗中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ca/10069701/dced4205324b/AJA-25-166-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ca/10069701/dced4205324b/AJA-25-166-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ca/10069701/dced4205324b/AJA-25-166-g001.jpg

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Andrologia. 2022 Aug;54(7):1581-1591. doi: 10.1111/and.14422. Epub 2022 Apr 12.
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METTL3-stabilized lncRNA SNHG7 accelerates glycolysis in prostate cancer via SRSF1/c-Myc axis.METTL3稳定的lncRNA SNHG7通过SRSF1/c-Myc轴促进前列腺癌的糖酵解。
Exp Cell Res. 2022 Jul 1;416(1):113149. doi: 10.1016/j.yexcr.2022.113149. Epub 2022 Apr 9.
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mA-induced repression of SIAH1 facilitates alternative splicing of androgen receptor variant 7 by regulating CPSF1.
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Oncol Rep. 2024 Jun;51(6). doi: 10.3892/or.2024.8747. Epub 2024 May 17.
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Cancers (Basel). 2023 Apr 11;15(8):2243. doi: 10.3390/cancers15082243.
毫安诱导的SIAH1抑制通过调节CPSF1促进雄激素受体变体7的可变剪接。
Mol Ther Nucleic Acids. 2022 Mar 15;28:219-230. doi: 10.1016/j.omtn.2022.03.008. eCollection 2022 Jun 14.
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