The Role of KH-Type Splicing Regulatory Protein (KSRP) for Immune Functions and Tumorigenesis.
KH-type splicing regulatory protein
T helper cell
antiviral response
cytokine
mRNA decay
micro RNA
post-transcriptional gene regulation
tumorigenesis
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
28 04 2022
28 04 2022
Historique:
received:
28
03
2022
revised:
21
04
2022
accepted:
26
04
2022
entrez:
14
5
2022
pubmed:
15
5
2022
medline:
18
5
2022
Statut:
epublish
Résumé
Post-transcriptional control of gene expression is one important mechanism that enables stringent and rapid modulation of cytokine, chemokines or growth factors expression, all relevant for immune or tumor cell function and communication. The RNA-binding protein KH-type splicing regulatory protein (KSRP) controls the mRNA stability of according genes by initiation of mRNA decay and inhibition of translation, and by enhancing the maturation of microRNAs. Therefore, KSRP plays a pivotal role in immune cell function and tumor progression. In this review, we summarize the current knowledge about KSRP with regard to the regulation of immunologically relevant targets, and the functional role of KSRP on immune responses and tumorigenesis. KSRP is involved in the control of myeloid hematopoiesis. Further, KSRP-mediated mRNA decay of pro-inflammatory factors is necessary to keep immune homeostasis. In case of infection, functional impairment of KSRP is important for the induction of robust immune responses. In this regard, KSRP seems to primarily dampen T helper cell 2 immune responses. In cancer, KSRP has often been associated with tumor growth and metastasis. In summary, aside of initiation of mRNA decay, the KSRP-mediated regulation of microRNA maturation seems to be especially important for its diverse biological functions, which warrants further in-depth examination.
Identifiants
pubmed: 35563788
pii: cells11091482
doi: 10.3390/cells11091482
pmc: PMC9104899
pii:
doi:
Substances chimiques
MicroRNAs
0
RNA-Binding Proteins
0
Trans-Activators
0
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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