The MSP-RON axis stimulates cancer cell growth in models of triple negative breast cancer.
Animals
Cell Line, Tumor
Cell Proliferation
Gene Expression Regulation, Neoplastic
Hepatocyte Growth Factor
/ metabolism
Humans
MAP Kinase Signaling System
Mice
Models, Biological
Proto-Oncogene Proteins
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
RNA, Messenger
/ genetics
Receptor Protein-Tyrosine Kinases
/ metabolism
Signal Transduction
Triple Negative Breast Neoplasms
/ genetics
MSP
MST1R
RON
breast cancer
mouse models
therapeutic target
Journal
Molecular oncology
ISSN: 1878-0261
Titre abrégé: Mol Oncol
Pays: United States
ID NLM: 101308230
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
19
02
2020
revised:
30
04
2020
accepted:
28
05
2020
pubmed:
3
6
2020
medline:
1
7
2021
entrez:
3
6
2020
Statut:
ppublish
Résumé
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor prognosis and high rates of relapse. The lack of actionable targets for TNBC has contributed to the high mortality rates of this disease, and new candidate molecules for potential manipulation are urgently required. Here, we show that macrophage-stimulating protein (MSP) and its tyrosine kinase receptor, Recepteur d'origine nantais (RON), are potent drivers of cancer cell growth and tumor progression in a mouse model of TNBC driven by the loss of Trp53 and Brca1. After comparison of two genetically engineered mouse models of TNBC, we found that mammary tumors from K14-Cre;Brca1
Identifiants
pubmed: 32484599
doi: 10.1002/1878-0261.12734
pmc: PMC7400785
doi:
Substances chimiques
Proto-Oncogene Proteins
0
RNA, Messenger
0
macrophage stimulating protein
0
Hepatocyte Growth Factor
67256-21-7
RON protein
EC 2.7.10.1
Receptor Protein-Tyrosine Kinases
EC 2.7.10.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1868-1880Subventions
Organisme : Cancer Research UK
ID : A25142
Pays : United Kingdom
Informations de copyright
© 2020 The Authors. Published by FEBS press John Wiley & Sons Ltd.
Références
Proc Natl Acad Sci U S A. 2007 May 1;104(18):7570-5
pubmed: 17456594
Cancer Discov. 2018 Mar;8(3):354-369
pubmed: 29203461
Oncogene. 1998 Jun 4;16(22):2927-33
pubmed: 9671413
Oncotarget. 2015 Jul 10;6(19):17445-61
pubmed: 25938541
Breast Cancer Res Treat. 2012 Dec;136(3):795-804
pubmed: 23124476
Clin Cancer Res. 2005 Mar 15;11(6):2222-8
pubmed: 15788670
Cancer Discov. 2013 Jul;3(7):751-60
pubmed: 23612011
Cell Rep. 2014 Jan 16;6(1):141-54
pubmed: 24388747
Oncoimmunology. 2018 Jul 11;7(9):e1480286
pubmed: 30228950
Nature. 2012 Apr 18;486(7403):346-52
pubmed: 22522925
Genes Cancer. 2011 Jul;2(7):753-62
pubmed: 22207901
Cancer Res. 2004 Aug 1;64(15):5154-61
pubmed: 15289319
Cancer Res. 2006 Dec 15;66(24):11967-74
pubmed: 17178895
Sci Transl Med. 2017 Jan 25;9(374):
pubmed: 28123075
Nat Rev Cancer. 2013 Jul;13(7):466-81
pubmed: 23792360
Nature. 2000 Aug 17;406(6797):747-52
pubmed: 10963602
Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12111-6
pubmed: 17626182
Nature. 2012 Oct 4;490(7418):61-70
pubmed: 23000897
Nat Rev Clin Oncol. 2016 Nov;13(11):674-690
pubmed: 27184417
Cancer Res. 2013 Jan 1;73(1):353-63
pubmed: 23151903
NPJ Breast Cancer. 2018 Nov 9;4:36
pubmed: 30456298