Dysregulated N6-methyladenosine (m6A) processing in hepatocellular carcinoma
N6-methyladenosine (m6A) is the most thoroughly studied type of internal RNA modification, as this epigenetic modification is the most abundant in eukaryotic RNAs to date. This modification occurs in various types of RNAs and plays significant roles in dominant RNA-related processes, such as translation, splicing, export and degradation.
Yue-fan Wang +6 more
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N6-methyladenosine (m6A) RNA modification in cancer stem cells [PDF]
Abstract Cancer stem cells (CSCs), a unique subset of undifferentiated cells with stem cell-like properties, have emerged as driving forces in mediating tumor growth, metastasis, and therapeutic resistance. Recent advances have highlighted that N6-methyladenosine (m6A) RNA modification plays an important role in cancer biology and CSCs ...
Zhonghua Ma, Jiafu Ji
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The emerging roles of N6-methyladenosine (m6A) deregulation in liver carcinogenesis [PDF]
AbstractLiver cancer is a common cancer worldwide. Although the etiological factors of liver carcinogenesis are well defined, the underlying molecular mechanisms remain largely elusive. Epigenetic deregulations, such as aberrant DNA methylation and histone modifications, play a critical role in liver carcinogenesis.
Mengnuo Chen, Chun-Ming Wong
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N6-methyladenosine (m6A) modification and its clinical relevance in cognitive dysfunctions [PDF]
N6 adenosine methylation (m6A) is the most abundant internal RNA modification in eukaryotic cells. Dysregulation of m6A has been associated with the perturbations of cell proliferation and cell death in different diseases. However, the roles of m6A in the neurodegenerative process and cognitive dysfunction are unclear.We systematically investigated the
Du, Bingying +8 more
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The emerging roles of N6-methyladenosine (m6A) deregulation in polycystic ovary syndrome. [PDF]
Abstract Polycystic ovary syndrome (PCOS) is an endocrine metabolic syndrome characterized by ovulation disorders, hyperandrogenemia, and polycystic ovaries, which seriously affect the psychological and physical health of childbearing women. N6-methyladenosine (m6A), as the most common mRNA epigenetic modification in eukaryotes, is vital for ...
Jiang L +13 more
europepmc +4 more sources
N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases. [PDF]
Fibrosis is an abnormal tissue healing process characterized by the excessive accumulation of ECM components, such as COL I and COL III, in response to tissue injury or chronic inflammation. Recent advances in epitranscriptomics have underscored the importance of m6A modification in fibrosis.
Tan M, Liu S, Liu L.
europepmc +4 more sources
N6-methyladenosine (m6A) modification in inflammation: a bibliometric analysis and literature review. [PDF]
N6-methyladenosine (m6A) is the most abundant internal messenger RNA modification in eukaryotes, influencing various physiological and pathological processes by regulating RNA metabolism. Numerous studies have investigated the role of m6A in inflammatory responses and inflammatory diseases.
Li Z +6 more
europepmc +5 more sources
Background: N6-methyladenosine (m6A) is the most extensive messenger RNA modification. Despite recent advances in the biological roles of m6A, its role in the development and progression of renal cell carcinoma (RCC) remains unclear.Methods: In this ...
Ying Gan +17 more
doaj +1 more source
N6-Methyladenosine modification: a novel pharmacological target for anti-cancer drug development
N6-Methyladenosine (m6A) modification is the most pervasive modification of human mRNA molecules. It is reversible via regulation of m6A modification methyltransferase, demethylase and proteins that preferentially recognize m6A modification as “writers”,
Yi Niu +4 more
doaj +1 more source
A neural m6A/Ythdf pathway is required for learning and memory in Drosophila
Epitranscriptomic modifications can regulate learning and memory. Here, the authors provide proteomic and functional analysis of N6-methyladenosine (m6A)-binding proteins in D.
Lijuan Kan +7 more
doaj +1 more source

