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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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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1724740044957155328 |