m6A RNA modification regulates innate lymphoid cell responses in a lineage-specific manner

Zhang, Yingyu; Zhang, Wanwei; Zhao, Jingyao; Ito, Takamasa; Jin, Jiacheng; Aparicio, Alexis O; Zhou, Junsong; Guichard, Vincent; Fang, Yinshan; Que, Jianwen; Urban, Joseph F.; Hanna, Jacob; Ghosh, Sankar; Wu, Xuebing; Ding, Lei; Basu, Uttiya; Huang, Yuandi

doi:10.1038/s41590-023-01548-4

Cited by 9 publications

(2 citation statements)

References 53 publications

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“…Through bioinformatic analyses and a literature search, METTL3 emerged as a potential methyltransferase closely related to craniofacial development. Operating within the methyltransferase complex in mammalian cells, METTL3 methylates its specific target transcripts and participates in various physiological processes encompassing embryonic development, brain development, and cell reprogramming [ 36 , 37 ]. Cai et al reported that METTL3 directly interacts with ACLY and SLC25A1, affecting the glycolytic pathway, and thus regulates the osteogenic differentiation of DPSCs [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

METTL3-dependent m6A modification of PSEN1 mRNA regulates craniofacial development through the Wnt/β-catenin signaling pathway

Ma,

Zhou,

Yao

et al. 2024

Cell Death Dis

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Craniofacial malformations, often associated with syndromes, are prevalent birth defects. Emerging evidence underscores the importance of m6A modifications in various bioprocesses such as stem cell differentiation, tissue development, and tumorigenesis. Here, in vivo, experiments with zebrafish models revealed that mettl3-knockdown embryos at 144 h postfertilization exhibited aberrant craniofacial features, including altered mouth opening, jaw dimensions, ethmoid plate, tooth formation and hypoactive behavior. Similarly, low METTL3 expression inhibited the proliferation and migration of BMSCs, HEPM cells, and DPSCs. Loss of METTL3 led to reduced mRNA m6A methylation and PSEN1 expression, impacting craniofacial phenotypes. Co-injection of mettl3 or psen1 mRNA rescued the level of Sox10 fusion protein, promoted voluntary movement, and mitigated abnormal craniofacial phenotypes induced by mettl3 knockdown in zebrafish. Mechanistically, YTHDF1 enhanced the mRNA stability of m6A-modified PSEN1, while decreased METTL3-mediated m6A methylation hindered β-catenin binding to PSEN1, suppressing Wnt/β-catenin signaling. Pharmacological activation of the Wnt/β-catenin pathway partially alleviated the phenotypes of mettl3 morphant and reversed the decreases in cell proliferation and migration induced by METTL3 silencing. This study elucidates the pivotal role of METTL3 in craniofacial development via the METTL3/YTHDF1/PSEN1/β-catenin signaling axis.

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Section: Discussionmentioning

confidence: 99%

METTL3-dependent m6A modification of PSEN1 mRNA regulates craniofacial development through the Wnt/β-catenin signaling pathway

Ma,

Zhou,

Yao

et al. 2024

Cell Death Dis

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“…Importantly, it is involved in the development and progression of various human diseases, including AML, CRC, GC, glioblastoma (GBM), renal cell carcinoma (RCC), HCC, etc. [28][29][30][31]. This paper will comprehensively explore the role of RNA methylation in tumor immunity and its potential applications in immunotherapy.…”

Section: Introductionmentioning

confidence: 99%

The role of RNA methylation in tumor immunity and its potential in immunotherapy

Li,

Jin,

et al. 2024

Mol Cancer

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RNA methylation, a prevalent post-transcriptional modification, has garnered considerable attention in research circles. It exerts regulatory control over diverse biological functions by modulating RNA splicing, translation, transport, and stability. Notably, studies have illuminated the substantial impact of RNA methylation on tumor immunity. The primary types of RNA methylation encompass N6-methyladenosine (m6A), 5-methylcytosine (m5C), N1-methyladenosine (m1A), and N7-methylguanosine (m7G), and 3-methylcytidine (m3C). Compelling evidence underscores the involvement of RNA methylation in regulating the tumor microenvironment (TME). By affecting RNA translation and stability through the "writers", "erasers" and "readers", RNA methylation exerts influence over the dysregulation of immune cells and immune factors. Consequently, RNA methylation plays a pivotal role in modulating tumor immunity and mediating various biological behaviors, encompassing proliferation, invasion, metastasis, etc. In this review, we discussed the mechanisms and functions of several RNA methylations, providing a comprehensive overview of their biological roles and underlying mechanisms within the tumor microenvironment and among immunocytes. By exploring how these RNA modifications mediate tumor immune evasion, we also examine their potential applications in immunotherapy. This review aims to provide novel insights and strategies for identifying novel targets in RNA methylation and advancing cancer immunotherapy efficacy.

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Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

Gao,

Lee,

Goodman

et al. 2024

Cell

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m6A RNA modification regulates innate lymphoid cell responses in a lineage-specific manner

Cited by 9 publications

References 53 publications

METTL3-dependent m6A modification of PSEN1 mRNA regulates craniofacial development through the Wnt/β-catenin signaling pathway

METTL3-dependent m6A modification of PSEN1 mRNA regulates craniofacial development through the Wnt/β-catenin signaling pathway

The role of RNA methylation in tumor immunity and its potential in immunotherapy

Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

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