The Tumor Suppressive mir-148a Is Epigenetically Inactivated in Classical Hodgkin Lymphoma.
Cell Line, Tumor
Cell Proliferation
/ genetics
DNA Methylation
Down-Regulation
/ genetics
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic
Genes, Tumor Suppressor
HEK293 Cells
Hodgkin Disease
/ genetics
Humans
MicroRNAs
/ genetics
Neoplasm Proteins
/ genetics
Promoter Regions, Genetic
Transcription, Genetic
DNA methylation
cHL
epigenetic
microRNA
mir-148a
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
14 10 2020
14 10 2020
Historique:
received:
24
09
2020
revised:
11
10
2020
accepted:
11
10
2020
entrez:
17
10
2020
pubmed:
18
10
2020
medline:
7
4
2021
Statut:
epublish
Résumé
DNA methylation was shown previously to be a crucial mechanism responsible for transcriptional deregulation in the pathogenesis of classical Hodgkin lymphoma (cHL). To identify epigenetically inactivated miRNAs in cHL, we have analyzed the set of miRNAs downregulated in cHL cell lines using bisulfite pyrosequencing. We focused on miRNAs with promoter regions located within or <1000 bp from a CpG island. Most promising candidate miRNAs were further studied in primary Hodgkin and Reed-Sternberg (HRS) cells obtained by laser capture microdissection. Last, to evaluate the function of identified miRNAs, we performed a luciferase reporter assay to confirm miRNA: mRNA interactions and therefore established cHL cell lines with stable overexpression of selected miRNAs for proliferation tests. We found a significant reverse correlation between DNA methylation and expression levels of mir-339-3p, mir-148a-3p, mir-148a-5p and mir-193a-5 demonstrating epigenetic regulation of these miRNAs in cHL cell lines. Moreover, we demonstrated direct interaction between miR-148a-3p and
Identifiants
pubmed: 33066457
pii: cells9102292
doi: 10.3390/cells9102292
pmc: PMC7602210
pii:
doi:
Substances chimiques
MIRN148 microRNA, human
0
MicroRNAs
0
Neoplasm Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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