Corrigendum: Why Be One Protein When You Can Affect Many? The Multiple Roles of YB-1 in Lung Cancer and Mesothelioma
Thomas G. Johnson
Karin Schelch
Sunali Mehta
Andrew Burgess
Glen Reid- 1Asbestos Diseases Research Institute, Sydney, NSW, Australia
- 2Cell Division Laboratory, The ANZAC Research Institute, Sydney, NSW, Australia
- 3School of Medicine, The University of Sydney, Sydney, NSW, Australia
- 4Sydney Catalyst Translational Cancer Research Centre, The University of Sydney, Sydney, NSW, Australia
- 5Institute of Cancer Research, Medical University of Vienna, Vienna, Austria
- 6Department of Pathology, University of Otago, Dunedin, New Zealand
- 7Maurice Wilkins Centre, University of Otago, Dunedin, New Zealand
A Corrigendum on
Why Be One Protein When You Can Affect Many? The Multiple Roles of YB-1 in Lung Cancer and Mesothelioma
by Johnson, T. G., Schelch, K., Mehta, S., Burgess, A., and Reid, G. (2019). Front. Cell Dev. Biol. 7:221. doi: 10.3389/fcell.2019.00221
In the original article, there was an error. The authors wrote “adenylation” instead of “acetylation”.
A correction has been made to the YB-1: a malignant jack of all trades section, subsection YB-1 is secreted into the extracellular space under cellular stress, paragraph two:
“Y-box binding protein-1 is related on an evolutionary level to HMGB1 and is also secreted under certain cellular stresses. This was first evident in monocytes stimulated with bacterial lipopolysaccharide through an active, non-classical pathway and appears to require the same two lysine residues (Lys301/304) that are the site of acetylation in hemodialysis patients (Frye et al., 2009; Ewert et al., 2018; Figures 3–5). Secreted YB-1 stimulated DNA synthesis, cell proliferation and migration of kidney cells (Frye et al., 2009). More pertinent to thoracic cancer, YB-1 is also secreted under oxidative stress. YB-1 translationally upregulates G3BP1 under oxidative stress and localizes to cytoplasmic stress granules where it is involved in pro-survival mRNA reprogramming (Somasekharan et al., 2015). G3BP1 also promotes the invasion and metastasis of sarcoma cells in vivo (Somasekharan et al., 2015). In support, YB-1 enrichment in stress granules is also linked to its secretion to the extracellular space under oxidizing conditions (Guarino et al., 2018; Figures 4, 5). Secretion of YB-1 resulted in depletion of cytoplasmic YB-1, leaving nuclear expression intact (presumably to allow for YB-1-mediated DNA repair), while secreted YB-1 inhibited the growth of neighboring keratinocytes (Guarino et al., 2018).”
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
References
Ewert, L., Fischer, A., Brandt, S., Scurt, F. G., Philipsen, L., Müller, A. J., et al. (2018). Cold shock Y-box binding protein-1 acetylation status in monocytes is associated with systemic inflammation and vascular damage. Atherosclerosis 278, 156–165. doi: 10.1016/j.atherosclerosis.2018.09.020
Frye, B. C., Halfter, S., Djudjaj, S., Muehlenberg, P., Weber, S., Raffetseder, U., et al. (2009). Y-box protein-1 is actively secreted through a non-classical pathway and acts as an extracellular mitogen. EMBO Rep. 10, 783–789. doi: 10.1038/embor.2009.81
Guarino, A., Troiano, A., Pizzo, E., Bosso, A., Vivo, M., Pinto, G., et al. (2018). Oxidative stress causes enhanced secretion of YB-1 Protein that restrains proliferation of receiving cells. Genes. 9:E513. doi: 10.3390/genes9100513
Keywords: lung cancer, mesothelioma, targeted therapy, biomarker, Y-box binding protein-1
Citation: Johnson TG, Schelch K, Mehta S, Burgess A and Reid G (2019) Corrigendum: Why Be One Protein When You Can Affect Many? The Multiple Roles of YB-1 in Lung Cancer and Mesothelioma. Front. Cell Dev. Biol. 7:293. doi: 10.3389/fcell.2019.00293
Received: 22 October 2019; Accepted: 06 November 2019;
Published: 22 November 2019.
Edited and reviewed by: Dominic C. Voon, Kanazawa University, Japan
Copyright © 2019 Johnson, Schelch, Mehta, Burgess and Reid. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Glen Reid, glen.reid@otago.ac.nz