4.4 Review

The role m6A RNA methylation is CNS development and glioma pathogenesis

Journal

MOLECULAR BRAIN
Volume 14, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s13041-021-00831-5

Keywords

Glioma; GBM; m(6)A methylation; METTL3; WTAP; ALKBH5; FTO

Categories

Funding

  1. National Natural Science Foundation of China [81502147]
  2. Zhejiang Medical Science and Technology Project [2017KY260, 2018KY292, 2019RC127, 2018KY291]
  3. Zhejiang Provincial National Science Foundation of China [LY21H160007, Y21H160038, Q18H290002, LQ20H290001]
  4. Youth Scientific Innovation Foundation of Zhejiang Cancer Hospital [QN201902]
  5. third term new medical talents of Zhejiang province project

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Epigenetic abnormalities, particularly RNA methylation, play a crucial role in tumors such as glioma. The m(6)A methylation, the most common form of RNA methylation, is closely associated with the occurrence and development of various tumors, including glioma. In-depth research on the mechanisms of m(6)A methylation may lead to the development of new therapeutic options for glioma based on the inhibition of m(6)A deposition.
Epigenetic abnormalities play a crucial role in many tumors, including glioma. RNA methylation occurs as an epigenetic modification similar to DNA methylation and histone modification. m(6)A methylation is the most common and most intensively studied RNA methylation, which can be found throughout the RNA life cycle and exert biological functions by affecting RNA metabolism. The m(6)A modification is primarily associated with three types of protease, which are encoded by the writer, eraser and reader genes, respectively. It has been shown that the m(6)A methylation has close connections with the occurrence and development of many tumors, including glioma. In this study, the concept and the research progress of m(6)A methylation are reviewed, especially the role of m(6)A methylation in glioma. Moreover, we will discuss how glioma is paving the way to the development of new therapeutic options based on the inhibition of m(6)A deposition.

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