Cargando…

FBXW7 in breast cancer: mechanism of action and therapeutic potential

Breast cancer is one of the frequent tumors that seriously endanger the physical and mental well-being in women. F-box and WD repeat domain-containing 7 (FBXW7) is a neoplastic repressor. Serving as a substrate recognition element for ubiquitin ligase, FBXW7 participates in the ubiquitin–proteasome...

Descripción completa

Detalles Bibliográficos
Autores principales: Chen, Siyu, Leng, Ping, Guo, Jinlin, Zhou, Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10474666/
https://www.ncbi.nlm.nih.gov/pubmed/37658431
http://dx.doi.org/10.1186/s13046-023-02767-1
_version_ 1785100549378539520
author Chen, Siyu
Leng, Ping
Guo, Jinlin
Zhou, Hao
author_facet Chen, Siyu
Leng, Ping
Guo, Jinlin
Zhou, Hao
author_sort Chen, Siyu
collection PubMed
description Breast cancer is one of the frequent tumors that seriously endanger the physical and mental well-being in women. F-box and WD repeat domain-containing 7 (FBXW7) is a neoplastic repressor. Serving as a substrate recognition element for ubiquitin ligase, FBXW7 participates in the ubiquitin–proteasome system and is typically in charge of the ubiquitination and destruction of crucial oncogenic proteins, further performing a paramount role in cell differentiation, apoptosis and metabolic processes. Low levels of FBXW7 cause abnormal stability of pertinent substrates, mutations and/or deletions in the FBXW7 gene have been reported to correlate with breast cancer malignant progression and chemoresistance. Given the lack of an effective solution to breast cancer's clinical drug resistance dilemma, elucidating FBXW7's mechanism of action could provide a theoretical basis for targeted drug exploration. Therefore, in this review, we focused on FBXW7's role in a range of breast cancer malignant behaviors and summarized the pertinent cellular targets, signaling pathways, as well as the mechanisms regulating FBXW7 expression. We also proposed novel perspectives for the exploitation of alternative therapies and specific tumor markers for breast cancer by therapeutic strategies aiming at FBXW7.
format Online
Article
Text
id pubmed-10474666
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-104746662023-09-03 FBXW7 in breast cancer: mechanism of action and therapeutic potential Chen, Siyu Leng, Ping Guo, Jinlin Zhou, Hao J Exp Clin Cancer Res Review Breast cancer is one of the frequent tumors that seriously endanger the physical and mental well-being in women. F-box and WD repeat domain-containing 7 (FBXW7) is a neoplastic repressor. Serving as a substrate recognition element for ubiquitin ligase, FBXW7 participates in the ubiquitin–proteasome system and is typically in charge of the ubiquitination and destruction of crucial oncogenic proteins, further performing a paramount role in cell differentiation, apoptosis and metabolic processes. Low levels of FBXW7 cause abnormal stability of pertinent substrates, mutations and/or deletions in the FBXW7 gene have been reported to correlate with breast cancer malignant progression and chemoresistance. Given the lack of an effective solution to breast cancer's clinical drug resistance dilemma, elucidating FBXW7's mechanism of action could provide a theoretical basis for targeted drug exploration. Therefore, in this review, we focused on FBXW7's role in a range of breast cancer malignant behaviors and summarized the pertinent cellular targets, signaling pathways, as well as the mechanisms regulating FBXW7 expression. We also proposed novel perspectives for the exploitation of alternative therapies and specific tumor markers for breast cancer by therapeutic strategies aiming at FBXW7. BioMed Central 2023-09-02 /pmc/articles/PMC10474666/ /pubmed/37658431 http://dx.doi.org/10.1186/s13046-023-02767-1 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Chen, Siyu
Leng, Ping
Guo, Jinlin
Zhou, Hao
FBXW7 in breast cancer: mechanism of action and therapeutic potential
title FBXW7 in breast cancer: mechanism of action and therapeutic potential
title_full FBXW7 in breast cancer: mechanism of action and therapeutic potential
title_fullStr FBXW7 in breast cancer: mechanism of action and therapeutic potential
title_full_unstemmed FBXW7 in breast cancer: mechanism of action and therapeutic potential
title_short FBXW7 in breast cancer: mechanism of action and therapeutic potential
title_sort fbxw7 in breast cancer: mechanism of action and therapeutic potential
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10474666/
https://www.ncbi.nlm.nih.gov/pubmed/37658431
http://dx.doi.org/10.1186/s13046-023-02767-1
work_keys_str_mv AT chensiyu fbxw7inbreastcancermechanismofactionandtherapeuticpotential
AT lengping fbxw7inbreastcancermechanismofactionandtherapeuticpotential
AT guojinlin fbxw7inbreastcancermechanismofactionandtherapeuticpotential
AT zhouhao fbxw7inbreastcancermechanismofactionandtherapeuticpotential