Research Progress on the Role of M6A Methylation Modification in the Genesis and Development of GC
Abstract
Modifcation of M6ARNAmethylation is the most prevalent form of RNAediting in eukaryotic organisms. The m6A-methylated regulatory protein is intimately associated with biological processes, including GC proliferation, invasion, and metastasis. This protein is anticipated to serve as a target for the clinical treatment of GC in the future. This comprehensive review delineates the most recent advance-ments and clinical implications of m6Aaberrant modifcation in GC, aiming to furnish a novel research avenue for the exploration of GC’s future direction.
References
[1] Sung, H., et al., Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in
185 Countries. CA Cancer J Clin, 2021. 71(3): p. 209-249.
[2] Zong, L., et al., The challenge of screening for early GC in China. Lancet, 2016. 388(10060): p. 2606.
[3] Asaka, M., et al., GC deaths by age group in Japan: Outlook on preventive measures for elderly adults. Cancer Sci, 2020. 111(10): p.3845-3853.
[4] Wang, S., et al., Global and national trends in the age-specific sex ratio of esophageal cancer and GC by subtype. Int J Cancer,
2022. 151(9): p. 1447-1461.
[5] Wang, F., et al., Family history of malignant tumor is a predictor of GC prognosis: Incorporation into a nomogram. Medicine (Baltimore), 2022. 101(35): p. e30141.
[6] Usui, Y., et al., Helicobacter pylori, Homologous-Recombination Genes, and GC. N Engl J Med, 2023. 388(13): p. 1181-1190.
[7] Comprehensive molecular characterization of gastric adenocarcinoma. Nature, 2014. 513(7517): p. 202-9.
[8] Nguyen, P.H., et al., Characterization of Biomarkers of Tumorigenic and Chemoresistant Cancer Stem Cells in Human Gastric Carcinoma. Clin Cancer Res, 2017. 23(6): p. 1586-1597.
[9] Lander, E.S., et al., Initial sequencing and analysis of the human genome. Nature, 2001. 409(6822): p. 860-921.
[10] Guan, K., et al., Expression Status And Prognostic Value Of M6A-associated Genes in GC. J Cancer, 2020. 11(10): p. 3027-3040.
[11] Liang, Z., et al., Epigenetic N6-methyladenosine modification of RNA and DNA regulates cancer. Cancer Biol Med, 2020. 17(1): p.
9-19.
[12] Melstrom, L. and J. Chen, RNA N(6)-methyladenosine modification in solid tumors: new therapeutic frontiers. Cancer Gene Ther,
2020. 27(9): p. 625-633.
[13] Weng, H., H. Huang, and J. Chen, RNA N (6)-Methyladenosine Modification in Normal and Malignant Hematopoiesis. Adv Exp
Med Biol, 2019. 1143: p. 75-93.
[14] Mauer, J. and S.R. Jaffrey, FTO, m(6) A(m), and the hypothesis of reversible epitranscriptomic mRNA modifications. FEBS Lett,
2018. 592(12): p. 2012-2022.
[15] Meyer, K.D. and S.R. Jaffrey, The dynamic epitranscriptome: N6-methyladenosine and gene expression control. Nat Rev Mol Cell
Biol, 2014. 15(5): p. 313-26.
[16] Wang, N., et al., METTL3-Mediated ADAMTS9 Suppression Facilitates Angiogenesis and Carcinogenesis in GC. Front Oncol,
2022. 12: p. 861807.
[17] Ji, G., X. Wang, and H. Xi, METTL3-mediated m(6)A modification of lncRNA SNHG3 accelerates GC progression by modulating miR-186-5p/cyclinD2 axis. Int J Immunopathol Pharmacol, 2023. 37: p. 3946320231204694.
[18] Li, R., et al., miR-181-5p/KLHL5 Promoted Proliferation and Migration of GC Through Activating METTL3-Mediated m6A Process. Mol Biotechnol, 2023.
[19] Liu, N., C. Zhang, and L. Zhang, WTAP-Involved the m6A Modification of lncRNA FAM83H-AS1 Accelerates the Development
of GC. Mol Biotechnol, 2023.
[20] Miao, R., et al., KIAA1429 regulates cell proliferation by targeting c-Jun messenger RNA directly in GC. J Cell Physiol, 2020.
235(10): p. 7420-7432.
[21] Wang, X.K., et al., METTL16 promotes cell proliferation by up-regulating cyclin D1 expression in GC. J Cell Mol Med, 2021.
25(14): p. 6602-6617.
[22] Fan, H.N., et al., METTL14-mediated m(6)A modification of circORC5 suppresses GC progression by regulating miR-30c-2-3p/
AKT1S1 axis. Mol Cancer, 2022. 21(1): p. 51.
[23] Liu, X., et al., The m6A methyltransferase METTL14 inhibits the proliferation, migration, and invasion of GC by regulating the
PI3K/AKT/mTOR signaling pathway. J Clin Lab Anal, 2021. 35(3): p. e23655.
[24] Zhu, Y., et al., Demethylase FTO enhances the PI3K/Akt signaling to promote GC malignancy. Med Oncol, 2023. 40(5): p. 130.
[25] Zhou, Y., et al., N6-methyladenosine demethylase FTO promotes growth and metastasis of GC via m(6)A modification of caveolin-1 and metabolic regulation of mitochondrial dynamics. Cell Death Dis, 2022. 13(1): p. 72.
[26] Hu, Y., et al., Demethylase ALKBH5 suppresses invasion of GC via PKMYT1 m6A modification. Mol Cancer, 2022. 21(1): p. 34.
[27] Chen, W., et al., PLAGL2 promotes Snail expression and GC progression via UCA1/miR-145-5p/YTHDF1 axis. Carcinogenesis, 2023. 44(4): p. 328-340.
[28] Bai, X., et al., Loss of YTHDF1 in gastric tumors restores sensitivity to antitumor immunity by recruiting mature dendritic cells. J
Immunother Cancer, 2022. 10(2).
[29] Shen, X., et al., YTHDF2 Inhibits GC Cell Growth by Regulating FOXC2 Signaling Pathway. Front Genet, 2020. 11: p. 592042.
[30] Ji, R., et al., IGF2BP2-meidated m(6)A modification of CSF2 reprograms MSC to promote GC progression. Cell Death Dis, 2023.
14(10): p. 693.
[31] Wang, Y., et al., METTL3 promotes drug resistance to oxaliplatin in GC cells through DNA repair pathway. Front Pharmacol,
2023. 14: p. 1257410.
[32] Tang, B., et al., N(6)-methyladenosine (m(6)A) writer KIAA1429 accelerates GC oxaliplatin chemoresistance by targeting
FOXM1. J Cancer Res Clin Oncol, 2023. 149(8): p. 5037-5045.
[33] Zhu, Z., et al., m(6)A Methyltransferase KIAA1429 Regulates the Cisplatin Sensitivity of GC Cells via Stabilizing FOXM1
mRNA. Cancers (Basel), 2022. 14(20).
[34] Liu, Y. and M. Da, Wilms tumor 1 associated protein promotes epithelial mesenchymal transition of GC cells by accelerating
TGF-β and enhances chemoradiotherapy resistance. J Cancer Res Clin Oncol, 2023. 149(7): p. 3977-3988.
Authors submitting to USP journals agree to publish their manuscript under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0) where authors agree to allow third parties to share their work (copy, distribute, transmit) and to adapt it, under the condition that the authors are given credit, and that in the event of reuse or distribution, the terms of this license are made clear
Authors retain copyright of their work, with first publication rights (online and print) granted to Universe Scientific Publishing or the owner of the journal in question.
