Comprehensive immunohistochemical analysis of N6-methyladenosine (m6A) writers, erasers, and readers in endometrial cancer.
Biomarker
Endometrial cancer
RNA modification
m6A
Journal
Journal of cancer research and clinical oncology
ISSN: 1432-1335
Titre abrégé: J Cancer Res Clin Oncol
Pays: Germany
ID NLM: 7902060
Informations de publication
Date de publication:
Jun 2023
Jun 2023
Historique:
received:
29
04
2022
accepted:
20
05
2022
medline:
27
4
2023
pubmed:
23
6
2022
entrez:
22
6
2022
Statut:
ppublish
Résumé
N6-methyladenosine (m6A) is the most frequent type of messenger RNA (mRNA) modification and is implicated in diverse physiological processes. The procedure of m6A RNA modification is regulated by a dynamic interaction of writers (METTL3, METTL4, METTL14, WTAP, KIAA1429), erasers (FTO, ALKBH5), and readers (HNRNPA2B1, HNRNPC, YTHDC1, YTHDC1, YTHDF1-3). In the oncological context, alterations in m6A were identified to be critically involved in tumorigenesis, proliferation, angiogenesis, and drug resistance across diverse cancer entities including endometrial cancer (EC). In this study, we comprehensively examined the protein expression of m6A writers, readers and erasers by immunohistochemical staining in a cohort of N = 65 EC patients. Protein expression data were analyzed with regard to clinical outcomes. We identified enhanced protein expression levels of METTL3, METTL14, FTO, HNRNPA2B1, and HNRNPC, respectively to be of prognostic value and linked to a shortened overall survival in EC. Overall, our study points toward dysregulated m6A modification in EC and its possibility to serve as a promising prognostic biomarker.
Identifiants
pubmed: 35731272
doi: 10.1007/s00432-022-04083-1
pii: 10.1007/s00432-022-04083-1
pmc: PMC10129960
doi:
Substances chimiques
Adenosine
K72T3FS567
METTL3 protein, human
EC 2.1.1.62
Methyltransferases
EC 2.1.1.-
FTO protein, human
EC 1.14.11.33
Alpha-Ketoglutarate-Dependent Dioxygenase FTO
EC 1.14.11.33
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2417-2424Subventions
Organisme : BONFOR
ID : 2021-1A-14
Organisme : BONFOR
ID : 2020-2A-12
Informations de copyright
© 2022. The Author(s).
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