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Review
. 2022 May 19;15(1):63.
doi: 10.1186/s13045-022-01285-5.

The potential role of N7-methylguanosine (m7G) in cancer

Yuejun Luo #  1   2 , Yuxin Yao #  1   2 , Peng Wu  1   2 , Xiaohui Zi  1   2 , Nan Sun  3   4 , Jie He  5   6
Affiliations
Review

The potential role of N7-methylguanosine (m7G) in cancer

Yuejun Luo et al. J Hematol Oncol. .

Abstract

N7-methylguanosine (m7G), one of the most prevalent RNA modifications, has recently attracted significant attention. The m7G modification actively participates in biological and pathological functions by affecting the metabolism of various RNA molecules, including messenger RNA, ribosomal RNA, microRNA, and transfer RNA. Increasing evidence indicates a critical role for m7G in human disease development, especially cancer, and aberrant m7G levels are closely associated with tumorigenesis and progression via regulation of the expression of multiple oncogenes and tumor suppressor genes. Currently, the underlying molecular mechanisms of m7G modification in cancer are not comprehensively understood. Here, we review the current knowledge regarding the potential function of m7G modifications in cancer and discuss future m7G-related diagnostic and therapeutic strategies.

Keywords: Cancer; N 7-methylguanosine (m7G); RNA metabolism; RNA modification.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The cellular m7G modification machinery. The m7G modification is a multilayered process. The m7G methyltransferases have been identified as METTL1, WDR4, RNMT, RAM, WBSCR22, and TMRT112, which install the m7G modification on target RNA molecules, including mRNA, tRNA, rRNA, and miRNA. The METTL1/WDR4 complex installs m7G modification on mRNA (internal site), tRNA (G46 site), and miRNA (G-quadruplex structure), ultimately regulating global translation. The RNMT/RAM complex is responsible for installation of the m7G modification on the 5’ cap of mRNA, mediating its nuclear export and translation processes. The WBSCR22/TMRT112 complex adds m7G modification at the G1638 site of 18 s rRNA, which facilitates 18 s rRNA maturation
Fig. 2
Fig. 2
The cross talk between m7G modification and other posttranscriptional modifications. The m6Am methyltransferase PCIF1 catalyzes m6Am modification adjacent to the m7G cap, which enhances resistance to DCP2-dominated decapping. The m6Am methyltransferase METTL14 installs m6Am modification at an internal site in U2 snRNA, ultimately influencing global alternative RNA splicing
Fig. 3
Fig. 3
The role of m7G regulators in various tumors. The m7G regulators are involved in tumor development and progression in different cancers, including AML, BC, CC, ESCC, glioma, HCC, HNSCC, ICC, LC, NPC, and PC. These m7G regulators play a dual role in various cancers, promoting or inhibiting tumor progression by regulating the expression of tumor-related genes
Fig. 4
Fig. 4
The gene and protein structures of METTL1 and WDR4. A The gene structures of METTL1 and WDR4. B The 3D structures of METTL1 and WDR4. The potential binding site was showed in rose red surface mode
See this image and copyright information in PMC

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