The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis.
The m(6)A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis.
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N6 -甲基腺苷（m(6)A）RNA甲基化调控致癌信号通路，驱动细胞恶性转化和致癌作用。
DOI：
10.1186/s12943-021-01356-0
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发表时间：
2021-04-04
期刊：
影响因子：
37.3
通讯作者：
Yang C
中科院分区：
文献类型：
--
作者：
Uddin MB;Wang Z;Yang C
m6 A RNA甲基化是哺乳动物mRNA中最普遍的内部修饰，通过调节重要的细胞过程发挥重要的生物学作用。由于其调节蛋白的异常表达而导致的m6 A修饰的失调经常在许多病理状况中观察到，特别是在癌症中。正常细胞通过复杂的机制激活或调节不同的致癌信号通路而发生恶性转化。越来越多的证据表明，在表转录组水平上调节致癌信号通路增加了一层额外的复杂性。特别是，最近的研究表明，在许多类型的癌症中，各种致癌信号传导途径受到靶mRNA以及非编码RNA转录物中m6 A修饰的调节。这些RNA分子中的m6 A修饰通过调节其稳定性、翻译或亚细胞定位来控制其命运和代谢。在这篇综述中，我们讨论了最近令人兴奋的研究致癌信号通路，调节m6 A RNA修饰和/或其调节剂在癌症中，并提供了进一步的研究前景。通过m6 A修饰及其调节剂对致癌信号传导途径的调节也使它们成为治疗癌症的潜在药物靶标。
The m6A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes. Dysregulations of the m6A modification due to aberrant expression of its regulatory proteins are frequently observed in many pathological conditions, particularly in cancer. Normal cells undergo malignant transformation via activation or modulation of different oncogenic signaling pathways through complex mechanisms. Accumulating evidence showing regulation of oncogenic signaling pathways at the epitranscriptomic level has added an extra layer of the complexity. In particular, recent studies demonstrated that, in many types of cancers various oncogenic signaling pathways are modulated by the m6A modification in the target mRNAs as well as noncoding RNA transcripts. m6A modifications in these RNA molecules control their fate and metabolism by regulating their stability, translation or subcellular localizations. In this review we discussed recent exciting studies on oncogenic signaling pathways that are modulated by the m6A RNA modification and/or their regulators in cancer and provided perspectives for further studies. The regulation of oncogenic signaling pathways by the m6A modification and its regulators also render them as potential druggable targets for the treatment of cancer.
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