Abstract
Recent studies have identified N6-methyladenosine (m6A) RNA methylation as a key regulatory mechanism in tumor progression. This study aimed to elucidate the biological function and clinical relevance of the m6A methyltransferase METTL3 in cutaneous T-cell lymphoma (CTCL). Our findings demonstrated that METTL3 expression is upregulated in CTCL, and its knockdown suppresses CTCL progression. Mechanistically, the downregulation of METTL3-mediated m6A modification on ARHGEF12 mRNA accelerated its degradation, a process that is closely associated with tumor behaviors. These results suggest that METTL3 may serve as a potential therapeutic target in CTCL.
Keywords:
ARHGEF12; METTL3; m6A.
MeSH terms
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Adenosine / analogs & derivatives
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Adenosine / metabolism
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Animals
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Cell Line, Tumor
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Cell Proliferation
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Disease Progression
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Female
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Gene Expression Regulation, Neoplastic*
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Humans
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Lymphoma, T-Cell, Cutaneous* / genetics
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Lymphoma, T-Cell, Cutaneous* / metabolism
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Lymphoma, T-Cell, Cutaneous* / pathology
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Male
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Methyltransferases* / genetics
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Methyltransferases* / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Rho Guanine Nucleotide Exchange Factors* / genetics
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Rho Guanine Nucleotide Exchange Factors* / metabolism
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Skin Neoplasms* / genetics
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Skin Neoplasms* / metabolism
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Skin Neoplasms* / pathology
Substances
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Methyltransferases
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METTL3 protein, human
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Rho Guanine Nucleotide Exchange Factors
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Adenosine
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N-methyladenosine
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RNA, Messenger