Opposite Roles of Tra2β and SRSF9 in the v10 Exon Splicing of CD44.
CD44
SRSF9
Tra2β
alternative splicing
v10
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
30 Oct 2020
30 Oct 2020
Historique:
received:
01
09
2020
revised:
09
10
2020
accepted:
14
10
2020
entrez:
4
11
2020
pubmed:
5
11
2020
medline:
5
11
2020
Statut:
epublish
Résumé
CD44 is a transmembrane glycoprotein involved in cell-cell and cell-matrix interactions. Several CD44 protein isoforms are generated in human through alternative splicing regulation of nine variable exons encoding for the extracellular juxta-membrane region. While the CD44 splicing variants have been described to be involved in cancer progression and development, the regulatory mechanism(s) underlying their production remain unclear. Here, we identify Tra2β and SRSF9 as proteins with opposite roles in regulating CD44 exon v10 splicing. While Tra2β promotes v10 inclusion, SRSF9 inhibits its inclusion. Mechanistically, we found that both proteins are able to target v10 exon, with GAAGAAG sequence being the binding site for Tra2β and AAGAC that for SRSF9. Collectively, our data add a novel layer of complexity to the sequential series of events involved in the regulation of CD44 splicing.
Identifiants
pubmed: 33143085
pii: cancers12113195
doi: 10.3390/cancers12113195
pmc: PMC7692347
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Ministry of Education and the National Research Foundation of Korea
ID : 2020R1A2C2004682
Organisme : the Ministry of Education and the National Research Foundation of Korea
ID : 2019R1I1A1A01057372
Organisme : the Ministry of Education and the National Research Foundation of Korea
ID : 2016R1A5A1007318
Organisme : GIST Research Institute (GRI) IIBR" grant funded by the GIST
ID : 2020
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