The Role of FBXW7 in Gynecologic Malignancies.
FBXW7
LncRNAs
epigenetic
gynecologic cancers
miRNAs
mutations
target therapy
ubiquitin-proteasome system
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
17 05 2023
17 05 2023
Historique:
received:
22
03
2023
revised:
28
04
2023
accepted:
15
05
2023
medline:
7
7
2023
pubmed:
6
7
2023
entrez:
6
7
2023
Statut:
epublish
Résumé
The F-Box and WD Repeat Domain Containing 7 (FBXW7) protein has been shown to regulate cellular growth and act as a tumor suppressor. This protein, also known as FBW7, hCDC4, SEL10 or hAGO, is encoded by the gene FBXW7. It is a crucial component of the Skp1-Cullin1-F-box (SCF) complex, which is a ubiquitin ligase. This complex aids in the degradation of many oncoproteins, such as cyclin E, c-JUN, c-MYC, NOTCH, and MCL1, via the ubiquitin-proteasome system (UPS). The FBXW7 gene is commonly mutated or deleted in numerous types of cancer, including gynecologic cancers (GCs). Such FBXW7 mutations are linked to a poor prognosis due to increased treatment resistance. Hence, detection of the FBXW7 mutation may possibly be an appropriate diagnostic and prognostic biomarker that plays a central role in determining suitable individualized management. Recent studies also suggest that, under specific circumstances, FBXW7 may act as an oncogene. There is mounting evidence indicating that the aberrant expression of FBXW7 is involved in the development of GCs. The aim of this review is to give an update on the role of FBXW7 as a potential biomarker and also as a therapeutic target for novel treatments, particularly in the management of GCs.
Identifiants
pubmed: 37408248
pii: cells12101415
doi: 10.3390/cells12101415
pmc: PMC10216672
pii:
doi:
Substances chimiques
F-Box-WD Repeat-Containing Protein 7
0
F-Box Proteins
0
Ubiquitin-Protein Ligases
EC 2.3.2.27
Ubiquitins
0
FBXW7 protein, human
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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