IGF2BP1 promotes SRF-dependent transcription in cancer in a m6A- and miRNA-dependent manner.
Adenosine
/ analogs & derivatives
Animals
Cell Line, Tumor
Disease-Free Survival
Female
Gene Expression Regulation, Neoplastic
/ genetics
Hep G2 Cells
Humans
Liver Neoplasms
/ genetics
Lung Neoplasms
/ genetics
Male
Mice
MicroRNAs
/ genetics
Ovarian Neoplasms
/ genetics
RNA-Binding Proteins
/ genetics
Serum Response Factor
/ genetics
Xenograft Model Antitumor Assays
Journal
Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011
Informations de publication
Date de publication:
10 01 2019
10 01 2019
Historique:
received:
29
06
2018
accepted:
17
10
2018
pubmed:
30
10
2018
medline:
29
8
2019
entrez:
30
10
2018
Statut:
ppublish
Résumé
The oncofetal mRNA-binding protein IGF2BP1 and the transcriptional regulator SRF modulate gene expression in cancer. In cancer cells, we demonstrate that IGF2BP1 promotes the expression of SRF in a conserved and N6-methyladenosine (m6A)-dependent manner by impairing the miRNA-directed decay of the SRF mRNA. This results in enhanced SRF-dependent transcriptional activity and promotes tumor cell growth and invasion. At the post-transcriptional level, IGF2BP1 sustains the expression of various SRF-target genes. The majority of these SRF/IGF2BP1-enhanced genes, including PDLIM7 and FOXK1, show conserved upregulation with SRF and IGF2BP1 synthesis in cancer. PDLIM7 and FOXK1 promote tumor cell growth and were reported to enhance cell invasion. Consistently, 35 SRF/IGF2BP1-dependent genes showing conserved association with SRF and IGF2BP1 expression indicate a poor overall survival probability in ovarian, liver and lung cancer. In conclusion, these findings identify the SRF/IGF2BP1-, miRNome- and m6A-dependent control of gene expression as a conserved oncogenic driver network in cancer.
Identifiants
pubmed: 30371874
pii: 5146196
doi: 10.1093/nar/gky1012
pmc: PMC6326824
doi:
Substances chimiques
IGF2BP1 protein, human
0
MicroRNAs
0
RNA-Binding Proteins
0
SRF protein, human
0
Serum Response Factor
0
N-methyladenosine
CLE6G00625
Adenosine
K72T3FS567
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
375-390Références
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