Dynamic Malignant Wave of Ribosome-Insulted Gut Niche via the Wnt-CTGF/CCN2 Circuit.

Biological Sciences Cancer Cell Biology Functional Aspects of Cell Biology

Journal

iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038

Informations de publication

Date de publication:
22 May 2020
Historique:
received: 22 11 2019
revised: 13 12 2019
accepted: 14 04 2020
pubmed: 4 5 2020
medline: 4 5 2020
entrez: 4 5 2020
Statut: ppublish

Résumé

Stress-driven ribosome dysfunction triggers an eIF2α-mediated integrated stress response to maintain cellular homeostasis. Among four key eIF2α kinases, protein kinase R (PKR) expression positively associates with poor prognoses for colorectal cancer (CRC) patients. We identified PKR-linked Wnt signaling networks that facilitate early inflammatory niche and epithelial-mesenchymal transitions of tumor tissues in response to ribosomal insults. However, the downstream Wnt signaling target fibrogenic connective tissue growth factor (CTGF/CCN2) regulates the nuclear translocation of β-catenin in a negative feedback manner. Moreover, dwindling expression of the Wnt/β-catenin pathway-regulator CTGF triggers noncanonical Wnt pathway-mediated exacerbation of intestinal cancer progression such as an increase in cancer stemness and acquisition of chemoresistance in the presence of ribosomal insults. The Wnt-CTGF-circuit-associated landscape of oncogenic signaling events was verified with clinical genomic profiling. This ribosome-associated wave of crosstalk between stress and oncogenes provides valuable insight into potential molecular interventions against intestinal malignancies.

Identifiants

pubmed: 32361596
pii: S2589-0042(20)30261-3
doi: 10.1016/j.isci.2020.101076
pmc: PMC7200318
pii:
doi:

Types de publication

Journal Article

Langues

eng

Pagination

101076

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests The authors have no conflicts of interest to disclose.

Références

J Immunol. 2016 Aug 1;197(3):847-58
pubmed: 27307561
Breast Cancer Res. 2012 Jan 19;14(1):202
pubmed: 22264257
Curr Pharm Des. 2015;21(10):1279-91
pubmed: 25506898
Nat Cell Biol. 2010 May;12(5):468-76
pubmed: 20418870
J Immunol. 2013 Jun 15;190(12):6501-10
pubmed: 23686487
Oncogene. 2003 Oct 16;22(46):7146-54
pubmed: 14562043
Int J Cancer. 2009 Jul 1;125(1):171-80
pubmed: 19350627
Toxicol Appl Pharmacol. 2012 Nov 15;265(1):10-8
pubmed: 23022514
Pol J Vet Sci. 2008;11(4):339-45
pubmed: 19227132
Toxicol Sci. 2012 Jan;125(1):116-25
pubmed: 22003189
Matrix Biol. 2018 Aug;68-69:44-66
pubmed: 29574063
Cell. 2008 May 16;133(4):704-15
pubmed: 18485877
Gastrointest Cancer Res. 2012 Jan;5(1):19-27
pubmed: 22574233
Toxicol Sci. 2015 Jun;145(2):372-82
pubmed: 25766886
Cell. 2006 Nov 3;127(3):469-80
pubmed: 17081971
Mol Cancer. 2017 Jan 30;16(1):8
pubmed: 28137272
Nat Cell Biol. 2002 Jun;4(6):408-15
pubmed: 11992112
Hepatology. 2009 Nov;50(5):1567-76
pubmed: 19676129
Cell. 2010 Apr 2;141(1):39-51
pubmed: 20371344
Physiol Genomics. 2014 Apr 1;46(7):223-44
pubmed: 24520152
Trends Cell Biol. 2009 Mar;19(3):119-29
pubmed: 19208479
J Mol Cell Biol. 2015 Apr;7(2):92-104
pubmed: 25735597
J Immunol. 2013 Nov 15;191(10):5170-81
pubmed: 24098051
RNA Biol. 2012 May;9(5):563-76
pubmed: 22614827
Cell. 2016 Mar 24;165(1):45-60
pubmed: 27015306
Mol Cell. 2010 Oct 22;40(2):228-37
pubmed: 20965418
PLoS One. 2012;7(5):e36044
pubmed: 22606244
Gastroenterology. 2011 Nov;141(5):1762-72
pubmed: 21889923
Food Chem Toxicol. 2004 May;42(5):817-24
pubmed: 15046828
J Infect Dis. 2008 Jul 1;198(1):143-9
pubmed: 18498239
Infect Immun. 2007 Apr;75(4):1745-50
pubmed: 17283086
Nature. 2005 Dec 8;438(7069):867-72
pubmed: 16341016
EMBO Rep. 2016 Oct;17(10):1374-1395
pubmed: 27629041
Oncogene. 2015 Apr 23;34(17):2178-2188
pubmed: 24954509
World J Gastroenterol. 2012 Jul 28;18(28):3635-61
pubmed: 22851857
Oncogene. 1999 Nov 1;18(45):6112-20
pubmed: 10557102
Trends Cancer. 2017 Feb;3(2):113-125
pubmed: 28718442
Cancer Discov. 2017 Oct;7(10):1069-1087
pubmed: 28923911
J Cell Commun Signal. 2018 Dec;12(4):625-629
pubmed: 30393824
Toxicol Appl Pharmacol. 2009 Oct 1;240(1):46-54
pubmed: 19591856
Cell Metab. 2016 Jun 14;23(6):1004-1012
pubmed: 27304502
Cell. 2013 Aug 29;154(5):1060-1073
pubmed: 23993096
Nature. 2011 Jun 08;475(7355):222-5
pubmed: 21654748
Oncogene. 2010 Aug 26;29(34):4741-51
pubmed: 20531305
Curr Pharmacol Rep. 2017 Jun;3(3):114-125
pubmed: 28642837
J Biol Chem. 2016 May 6;291(19):10173-83
pubmed: 26961878
Cancer Lett. 2015 Mar 28;358(2):124-135
pubmed: 25462858
Proteomics. 2006 Jul;6(13):3926-37
pubmed: 16739128
Int J Cancer. 2016 Nov 1;139(9):2033-46
pubmed: 27389473
Cell. 2010 Mar 19;140(6):883-99
pubmed: 20303878
Toxins (Basel). 2014 Dec 16;6(12):3406-25
pubmed: 25521494
Mol Cancer. 2010 Aug 06;9:212
pubmed: 20691072
EMBO Mol Med. 2009 Sep;1(6-7):303-14
pubmed: 20049734

Auteurs

Ki Hyung Kim (KH)

Laboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences, Pusan National University, Yangsan 50612, Korea; Department of Obstetrics and Gynecology, Pusan National University College of Medicine, Busan 49241, Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, 49241, Korea.

Seung Joon Lee (SJ)

Laboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences, Pusan National University, Yangsan 50612, Korea.

Juil Kim (J)

Laboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences, Pusan National University, Yangsan 50612, Korea.

Yuseok Moon (Y)

Laboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences, Pusan National University, Yangsan 50612, Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, 49241, Korea. Electronic address: moon@pnu.edu.

Classifications MeSH