Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?

Endoplasmic reticulum glycoprotein folding quality control (ERQC) and ER-associated degradation (ERAD) preside over cellular glycoprotein secretion and maintain steady glycoproteostasis. When cells turn malignant, cancer cell plasticity is affected and supported either by point mutations, preferenti...

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Main Authors: Gábor Tax, Andrea Lia, Angelo Santino, Pietro Roversi
Format: Article
Language:English
Published: Hindawi Limited 2019-01-01
Series:Journal of Oncology
Online Access:http://dx.doi.org/10.1155/2019/8384913
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spelling doaj-1f67a9edbfc24c51bb3a87a727636dcc2020-11-25T02:50:07ZengHindawi LimitedJournal of Oncology1687-84501687-84692019-01-01201910.1155/2019/83849138384913Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?Gábor Tax0Andrea Lia1Angelo Santino2Pietro Roversi3Leicester Institute of Structural and Chemical Biology, Department of Molecular and Cell Biology, University of Leicester, Henry Wellcome Building, Lancaster Road, Leicester LE1 7RH, UKLeicester Institute of Structural and Chemical Biology, Department of Molecular and Cell Biology, University of Leicester, Henry Wellcome Building, Lancaster Road, Leicester LE1 7RH, UKInstitute of Sciences of Food Production, C.N.R. Unit of Lecce, via Monteroni, I-73100 Lecce, ItalyLeicester Institute of Structural and Chemical Biology, Department of Molecular and Cell Biology, University of Leicester, Henry Wellcome Building, Lancaster Road, Leicester LE1 7RH, UKEndoplasmic reticulum glycoprotein folding quality control (ERQC) and ER-associated degradation (ERAD) preside over cellular glycoprotein secretion and maintain steady glycoproteostasis. When cells turn malignant, cancer cell plasticity is affected and supported either by point mutations, preferential isoform selection, altered expression levels, or shifts to conformational equilibria of a secreted glycoprotein. Such changes are crucial in mediating altered extracellular signalling, metabolic behavior, and adhesion properties of cancer cells. It is therefore conceivable that interference with ERQC and/or ERAD can be used to selectively damage cancers. Indeed, inhibitors of the late stages of ERAD are already in the clinic against cancers such as multiple myeloma. Here, we review recent advances in our understanding of the complex relationship between glycoproteostasis and cancer biology and discuss the potential of ERQC and ERAD modulators for the selective targeting of cancer cell plasticity.http://dx.doi.org/10.1155/2019/8384913
collection DOAJ
language English
format Article
sources DOAJ
author Gábor Tax
Andrea Lia
Angelo Santino
Pietro Roversi
spellingShingle Gábor Tax
Andrea Lia
Angelo Santino
Pietro Roversi
Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?
Journal of Oncology
author_facet Gábor Tax
Andrea Lia
Angelo Santino
Pietro Roversi
author_sort Gábor Tax
title Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?
title_short Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?
title_full Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?
title_fullStr Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?
title_full_unstemmed Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?
title_sort modulation of erqc and erad: a broad-spectrum spanner in the works of cancer cells?
publisher Hindawi Limited
series Journal of Oncology
issn 1687-8450
1687-8469
publishDate 2019-01-01
description Endoplasmic reticulum glycoprotein folding quality control (ERQC) and ER-associated degradation (ERAD) preside over cellular glycoprotein secretion and maintain steady glycoproteostasis. When cells turn malignant, cancer cell plasticity is affected and supported either by point mutations, preferential isoform selection, altered expression levels, or shifts to conformational equilibria of a secreted glycoprotein. Such changes are crucial in mediating altered extracellular signalling, metabolic behavior, and adhesion properties of cancer cells. It is therefore conceivable that interference with ERQC and/or ERAD can be used to selectively damage cancers. Indeed, inhibitors of the late stages of ERAD are already in the clinic against cancers such as multiple myeloma. Here, we review recent advances in our understanding of the complex relationship between glycoproteostasis and cancer biology and discuss the potential of ERQC and ERAD modulators for the selective targeting of cancer cell plasticity.
url http://dx.doi.org/10.1155/2019/8384913
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