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Modulation of ERQC and ERAD: a broad-spectrum spanner in the works of cancer cells?

journal contribution
posted on 27.08.2019, 16:19 by Gábor Tax, Andrea Lia, Angelo Santino, Pietro Roversi
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.

Funding

P.R. is the recipient of a LISCB Wellcome Trust ISSF award, grant reference 204801/Z/16/Z. G.T. is funded by a Wellcome Trust Seed Award in Science to P.R., grant reference 214090/Z/18/Z. A.L. is the recipient of an Italian Government PhD Studentship.

History

Citation

Journal of Oncology, Volume 2019 |Article ID 8384913 | https://doi.org/10.1155/2019/8384913

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES/Biological Sciences/Molecular & Cell Biology

Version

VoR (Version of Record)

Published in

Journal of Oncology

Volume

2019

Publisher

Hindawi

issn

1687-8450

Acceptance date

27/08/2019

Copyright date

2019

Available date

01/10/2019

Notes

Erratum to Review article included.

Language

en

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