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
1
EwertL.FischerA.BrandtS.ScurtF. G.PhilipsenL.MüllerA. J.et al. (2018). Cold shock Y-box binding protein-1 acetylation status in monocytes is associated with systemic inflammation and vascular damage. Atherosclerosis278, 156–165. 10.1016/j.atherosclerosis.2018.09.020
2
FryeB. C.HalfterS.DjudjajS.MuehlenbergP.WeberS.RaffetsederU.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. 10.1038/embor.2009.81
3
GuarinoA.TroianoA.PizzoE.BossoA.VivoM.PintoG.et al. (2018). Oxidative stress causes enhanced secretion of YB-1 Protein that restrains proliferation of receiving cells. Genes.9:E513. 10.3390/genes9100513
4
SomasekharanS. P.El-NaggarA.LeprivierG.ChengH.HajeeS.GrunewaldT. G.et al. (2015). YB-1 regulates stress granule formation and tumor progression by translationally activating G3BP1. J. Cell Biol.208, 913–929. 10.1083/jcb.201411047
Summary
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
Volume
7 - 2019
Edited and reviewed by
Dominic C. Voon, Kanazawa University, Japan
Updates
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
This article was submitted to Cell Growth and Division, a section of the journal Frontiers in Cell and Developmental Biology
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