-Methyladenosine (mA) modification is the most pervasive modification of human mRNA molecules. It is reversible regulation of mA modification methyltransferase, demethylase and proteins that preferentially recognize mA modification as "writers", "erasers" and "readers", respectively. Altered expression levels of the mA modification key regulators substantially affect their function, leading to significant phenotype changes in the cell and organism. Recent studies have proved that the mA modification plays significant roles in regulation of metabolism, stem cell self-renewal, and metastasis in a variety of human cancers. In this review, we describe the potential roles of mA modification in human cancers and summarize their underlying molecular mechanisms. Moreover, we will highlight potential therapeutic approaches by targeting the key mA modification regulators for cancer drug development.
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http://dx.doi.org/10.1016/j.apsb.2018.06.001 | DOI Listing |
Plants (Basel)
December 2024
State Key Laboratory of Tree Genetics and Breeding, Nanjing Forestry University, Nanjing 210037, China.
-methyladenosine (mA) is a widespread post-transcriptional modification of RNA in eukaryotes. The conserved YTH-domain-containing RNA binding protein has been widely reported to serve as a typical mA reader in various species. However, no studies have reported the mA readers in ().
View Article and Find Full Text PDFNat Neurosci
January 2025
Department of Neurobiology & Behavior, University of California, Irvine, Irvine, CA, USA.
Huntington's disease (HD) is caused by a CAG repeat expansion in the HTT gene, leading to altered gene expression. However, the mechanisms leading to disrupted RNA processing in HD remain unclear. Here we identify TDP-43 and the N6-methyladenosine (m6A) writer protein METTL3 to be upstream regulators of exon skipping in multiple HD systems.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, No. 350 Longzihu Road, Xinzhan District, Hefei, 230012, Anhui, China.
Objective: Arthritis is a class of diseases, characterized by joint and surrounding inflammation, accompanied by joint swelling, pain, dysfunction. According to different factors, arthritis can be divided into osteoarthritis, rheumatoid arthritis, ankylosing spondylitis and so on. N6-methyladenosine (m6A) is the most common internal modification of eukaryotic mRNA and is involved in splicing, stabilization, output and degradation of RNA metabolism.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
January 2025
Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Long noncoding RNA (lncRNA) and N6-methyladenosine (m6A) methylation modification have recently been suggested as potential functional modulators in ovarian endometriosis, however, the function and mechanism of m6A-modified lncRNA in ovarian endometriosis remain poorly understood. In this study, we demonstrated that lncRNA UBOX5-AS1 expression was significantly elevated in ovarian endometriosis tissue and primary ectopic endometrial stromal cells. The expression of lncRNA UBOX5-AS1, which has m6A modifications, was highly positively correlated with demethylase Alk B homologous protein 5 (ALKBH5) expression and autophagy.
View Article and Find Full Text PDFCancer Lett
January 2025
Department of Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282 China. Electronic address:
N-methyladenosine (m6A) methylation, is a well-known epigenetic modification involved in various biological processes, including tumorigenesis. However, the role of AlkB homolog 5 (ALKBH5), a critical component of m6A modification, remains unclear in glioma. This study investigates the function of ALKBH5 in glioma progression and its potential as a therapeutic target.
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