3
IRUS Total
Downloads
  Altmetric

UCHL1 as a novel target in breast cancer: emerging insights from cell and chemical biology

File Description SizeFormat 
s41416-021-01516-5.pdfPublished version936.05 kBAdobe PDFView/Open
Title: UCHL1 as a novel target in breast cancer: emerging insights from cell and chemical biology
Authors: Mondal, M
Conole, D
Nautiyal, J
Tate, E
Item Type: Journal Article
Abstract: Breast cancer has the highest incidence and death rate among cancers in women worldwide. In particular, metastatic Estrogen Receptor negative (ER–) breast cancer and Triple-Negative Breast Cancer (TNBC) subtypes have very limited treatment options, with low survival rates. Ubiquitin carboxyl terminal hydrolase L1 (UCHL1), a ubiquitin C-terminal hydrolase belonging to the deubiquitinase (DUB) family of enzymes, is highly expressed in these cancer types, and several key reports have revealed emerging and important roles for UCHL1 in breast cancer. However, selective and potent small molecule UCHL1 inhibitors have been disclosed only very recently, alongside chemical biology approaches to detect regulated UHCL1 activity in cancer cells. These tools will enable novel insights into oncogenic mechanisms driven by UCHL1, and identification of substrate proteins deubiquitinated by UCHL1, with the ultimate goal of realizing the potential of UCHL1 as a drug target in breast cancer.
Issue Date: 1-Jan-2022
Date of Acceptance: 9-Jun-2021
URI: http://hdl.handle.net/10044/1/90377
DOI: 10.1038/s41416-021-01516-5
ISSN: 0007-0920
Publisher: Springer Nature [academic journals on nature.com]
Start Page: 24
End Page: 33
Journal / Book Title: British Journal of Cancer
Volume: 126
Copyright Statement: © The Author(s) 2021. 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.
Sponsor/Funder: Commission of the European Communities
Pfizer Incorporated
Funder's Grant Number: 840690
n/a
Keywords: Science & Technology
Life Sciences & Biomedicine
Oncology
GROWTH-FACTOR RECEPTOR
TERMINAL HYDROLASE L1
UBIQUITIN-PROTEASOME PATHWAY
TYROSINE KINASE INHIBITORS
ACTIVATED PROTEIN-KINASE
ESTROGEN-RECEPTOR
MESSENGER-RNA
LUNG-CANCER
PGP9.5 METHYLATION
IMMUNE-RESPONSE
1112 Oncology and Carcinogenesis
1117 Public Health and Health Services
Oncology & Carcinogenesis
Publication Status: Published
Online Publication Date: 2021-09-08
Appears in Collections:Chemistry
Biological and Biophysical Chemistry
Faculty of Natural Sciences



This item is licensed under a Creative Commons License Creative Commons