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Review
. 2024 Jan 30;22(1):79.
doi: 10.1186/s12964-023-01401-z.

Research progress of N1-methyladenosine RNA modification in cancer

Affiliations
Review

Research progress of N1-methyladenosine RNA modification in cancer

Yafeng Liu et al. Cell Commun Signal. .

Abstract

N1-methyladenosine (m1A) is a post-transcriptionally modified RNA molecule that plays a pivotal role in the regulation of various biological functions and activities. Especially in cancer cell invasion, proliferation and cell cycle regulation. Over recent years, there has been a burgeoning interest in investigating the m1A modification of RNA. Most studies have focused on the regulation of m1A in cancer enrichment areas and different regions. This review provides a comprehensive overview of the methodologies employed for the detection of m1A modification. Furthermore, this review delves into the key players in m1A modification, known as the "writers," "erasers," and "readers." m1A modification is modified by the m1A methyltransferases, or writers, such as TRMT6, TRMT61A, TRMT61B, TRMT10C, NML, and, removed by the demethylases, or erasers, including FTO and ALKBH1, ALKBH3. It is recognized by m1A-binding proteins YTHDF1, TYHDF2, TYHDF3, and TYHDC1, also known as "readers". Additionally, we explore the intricate relationship between m1A modification and its regulators and their implications for the development and progression of specific types of cancer, we discuss how m1A modification can potentially facilitate the discovery of novel approaches for cancer diagnosis, treatment, and prognosis. Our summary of m1A methylated adenosine modification detection methods and regulatory mechanisms in various cancers provides useful insights for cancer diagnosis, treatment, and prognosis. Video Abstract.

Keywords: Detect method; Erasers; N1-methyladenosine; Readers; Regulation of cancer; Writers.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
The techniques used for progressive renewal include ALKBH, immunoprecipitation, TGIRT-RT, and Dimroth arrangement. A. ARM-seq (ALKBH). B. m1A-ID-seq (ALKBH, immunoprecipitation). C. MeRIP-seq (ALKBH, immunoprecipitation, TGIRT-RT, and Dimroth arrangement). D. m1A-MAP (ALKBH, immunoprecipitation, and TGIRT-RT)
Fig. 2
Fig. 2
Detection of m1A modification. The stepwise updating techniques include more specific anti-m1A antibody IP, increasing the m1A fragment quant in RNA, and SS-RT, with a higher truncation rate, and TGIRT-RT, with a higher misincorporation rate, respectively. A m1A-IP-seq (IP). B m1A-quant-seq (quant). C m1A-seq-TGIRT and m1A-seq-SS (SS-RT and TGIRT-SS)
Fig. 3
Fig. 3
Regulators of m1A modification include writers, readers, and erasers. The expression of writers affects the occurrence of cancer. ALKBH3 regulates the proliferation of cancer through tDRs and tRFs. A Regulatory factors of RNA, including writers, erasers, and readers. B The regulatory mechanism of m1A in lung cancer (1) (writer). C The regulatory mechanism of m1A in lung cancer (2) (ALKBH3)
Fig. 4
Fig. 4
TRMT6/61A regulates BC and affects UPR, and ALKBH3 regulates the NOX/ROS signaling axis to affect tumor angiogenesis and invasiveness. A TRMT6/61A and BC (UPR). B ALKBH3 and BC (NOX/ROS). The m1A regulator ALKBH3 regulates the development of breast cancer and ovarian cancer through CSF-1. TRMT6 regulates the development of ovarian cancer through miR-191-5p. C The regulatory mechanism of m1A in ovarian cancer and breast cancer (ALKBH3). D The regulatory mechanism of m1A in ovarian cancer (TRMT6)
Fig. 5
Fig. 5
ALKBH1 promotes CRC development by regulating SMAD7 and MFAP2, whereas ALKBH1 plays a robust regulatory role in PC. A The regulatory mechanism of m1A in CRC. B The regulatory mechanism of m1A in PC. glioma progresses through the upstream ABCC3 gene, whereas HCC progresses through a downstream signaling pathway regulated by TRMT61/TRMT6T. C The ABCC3 gene controls the proliferation of cancer cells by regulating the m1A regulator. D The regulatory mechanism of m1A in HCC

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