N6‐methyladenosine functions and its role in skin cancer

N6‐methyladenosine (m6A) methylation is the most abundant mammalian mRNA modification. m6A regulates RNA processing, splicing, nucleation, translation and stability by transferring, removing and recognizing m6A methylation sites, which are critical for cancer initiation, progression, metabolism and...

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Published inExperimental dermatology Vol. 32; no. 1; pp. 4 - 12
Main Authors Ran, Yanqin, Yan, Zhuoxian, Jiang, Bimei, Liang, Pengfei
Format Journal Article
LanguageEnglish
Published Denmark Wiley Subscription Services, Inc 01.01.2023
Subjects
Adenosine - genetics
Adenosine - metabolism
Animals
Humans
Malignancy
Mammals
Melanoma
Metastases
Methylation
molecular mechanisms
mRNA
N6-methyladenosine
RNA epigenetics
RNA modification
RNA processing
Skin cancer
Skin Neoplasms - genetics
Tumors
skin cancer
molecular mechanisms
N6-methyladenosine
RNA epigenetics
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Summary:N6‐methyladenosine (m6A) methylation is the most abundant mammalian mRNA modification. m6A regulates RNA processing, splicing, nucleation, translation and stability by transferring, removing and recognizing m6A methylation sites, which are critical for cancer initiation, progression, metabolism and metastasis. m6A is involved in pathophysiological tumour development by altering m6A modification and expression levels in tumour oncogenes and suppressor genes. Skin cancers are by far the most common malignancies in humans, with well over a million cases diagnosed each year. Skin cancers are grouped into two main categories: melanoma and non‐melanoma skin cancers (NMSC), based on cell origin and clinical behaviour. In this review, we summarize m6A methylation functions in different skin cancers, and discuss how m6A methylation is involved in disease development and progression. Moreover, we review potential prognostic biomarkers and molecular targets for early skin cancer diagnosis and treatment.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.14696