The role of RNA methyltransferase METTL3 in gynecologic cancers: Results and mechanisms

Abstract

N6-methyladenosine (m6A) methylation is the most prevalent mRNA modification in eukaryotes, and it is defined as the methylation of nitrogen atoms on the six adenine (A) bases of RNA in the presence of methyltransferases. Methyltransferase-like 3 (Mettl3), one of the components of m6A methyltransferase, plays a decisive catalytic role in m6A methylation. Recent studies have confirmed that m6A is associated with a wide spectrum of biological processes and it significantly affects disease progression and prognosis of patients with gynecologic tumors, in which the role of Mettl3 cannot be ignored. Mettl3 is involved in numerous pathophysiological functions, such as embryonic development, fat accumulation, and tumor progression. Moreover, Mettl3 may serve as a potential target for treating gynecologic malignancies, thus, it may benefit the patients and prolong survival. However, there is a need to further study the role and mechanism of Mettl3 in gynecologic malignancies. This paper reviews the recent progression on Mettl3 in gynecologic malignancies, hoping to provide a reference for further research.

Exploring m6A‐RNA methylation as a potential therapeutic strategy for acute lung injury and acute respiratory distress syndrome

“…METTL3 and METTL14 act as m6A regulators that can affect the progression of different human pathologies through oncogenic or suppressive methods. In several human cancers, for example, METTL3 plays an oncogenic role by upregulating oncogenes that support tumor progression 20 . Conversely, METTL3 also behaves as a suppressor in the central nervous system (CNS), for example, by upregulating tumor suppressor genes as well as genes that promote synaptic damage 21 .…”

“…In several human cancers, for example, METTL3 plays an oncogenic role by upregulating oncogenes that support tumor progression. 20 Conversely, METTL3 also behaves as a suppressor in the central nervous system (CNS), for example, by upregulating tumor suppressor genes as well as genes that promote synaptic damage. 21 These observations in the literature highlight the fact that METTL3-METTL14 are not globally uniform but rather, their roles in m6A modification produce specific downstream events based on the site of interest.…”

METTL3 as a novel diagnosis and treatment biomarker and its association with glycolysis, cuproptosis and ceRNA in oesophageal carcinoma

“…[5][6][7][8][9][10][11][12][13] By regulating the m6A modification level of the target gene, METTL3 can affect the translation efficiency and post transcriptional modification of mRNA, thereby having a significant impact on cell function and physiological processes. 14,15 Research has shown that METTL3 is overexpressed in various tumours and is closely related to the biological behaviours of tumour cell proliferation, invasion and metastasis. [16][17][18][19][20][21][22] In previous studies, 23 we found that METTL3 is overexpressed in ESCA, and its expression level is closely related to 18 F-FDG PET/CT metabolic parameters.…”

“…As a core component of m6A methylation, Methyltransferase 3 and N6‐Adenosine‐Methyltransferase Complex Catalytic Subunit (METTL3) is involved in the regulation of various biological processes, including cell proliferation, differentiation and metabolism 5–13 . By regulating the m6A modification level of the target gene, METTL3 can affect the translation efficiency and post transcriptional modification of mRNA, thereby having a significant impact on cell function and physiological processes 14,15 . Research has shown that METTL3 is overexpressed in various tumours and is closely related to the biological behaviours of tumour cell proliferation, invasion and metastasis 16–22 .…”