Corrigendum: "Why Be One Protein When You Can Affect Many? The Multiple Roles of YB-1 in Lung Cancer and Mesothelioma"
- 1Asbestos Diseases Research Foundation, Australia
- 2Anzac Research Institute, Australia
- 3School of Medical Sciences, The University of Sydney, Australia
- 4Sydney Catalyst Translational Research Centre, University of Sydney, Australia
- 5Institute of Cancer Research, Department of Internal Medicine I, Medical University of Vienna, Austria
- 6Department of Pathology, Dunedin School of Medicine, University of Otago, New Zealand
- 7Maurice Wilkins Centre, New Zealand
In the original article, there was an error. On page 15 of the manuscript (PDF) we have written "adenylation" instead of "acetylation": "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 adenylation in hemodialysis patients (Frye et al., 2009;Ewert et al., 2018;Figures 3-5)". . A correction has been made to Section: YB-1: a malignant jack of all trades, Subsection: YB-1 is secreted into the extracellular space under cellular stress, Paragraph 2:Corrected paragraph: 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 YB1 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).
Keywords: lung cancer, Mesothelioma, targeted therapy, biomarker, Y-box binding protein-1
Received: 22 Oct 2019;
Accepted: 06 Nov 2019.
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: Prof. Glen Reid, Maurice Wilkins Centre, Auckland, Auckland, New Zealand, email@example.com