(Phospho)proteomic Profiling of Microsatellite Unstable CRC Cells Reveals Alterations in Nuclear Signaling and Cholesterol Metabolism Caused by Frameshift Mutation of NMD Regulator UPF3A.
DNA mismatch repair
MSI tumorigenesis
UPF3A
coding mononucleotide repeats
nonsense-mediated RNA decay
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
23 Jul 2020
23 Jul 2020
Historique:
received:
09
06
2020
revised:
13
07
2020
accepted:
20
07
2020
entrez:
29
7
2020
pubmed:
29
7
2020
medline:
17
2
2021
Statut:
epublish
Résumé
DNA mismatch repair-deficient colorectal cancers (CRCs) accumulate numerous frameshift mutations at repetitive sequences recognized as microsatellite instability (MSI). When coding mononucleotide repeats (cMNRs) are affected, tumors accumulate frameshift mutations and premature termination codons (PTC) potentially leading to truncated proteins. Nonsense-mediated RNA decay (NMD) can degrade PTC-containing transcripts and protect from such faulty proteins. As it also regulates normal transcripts and cellular physiology, we tested whether NMD genes themselves are targets of MSI frameshift mutations. A high frequency of cMNR frameshift mutations in the
Identifiants
pubmed: 32718059
pii: ijms21155234
doi: 10.3390/ijms21155234
pmc: PMC7432364
pii:
doi:
Substances chimiques
Neoplasm Proteins
0
Phosphoproteins
0
RNA-Binding Proteins
0
UPF3A protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Krebshilfe
ID : 592/6-2
Organisme : Deutsche Forschungsgemeinschaft
ID : 110121
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