FGFR1 and FGFR4 oncogenicity depends on n-cadherin and their co-expression may predict FGFR-targeted therapy efficacy.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Mar 2020
Historique:
received: 09 10 2019
revised: 05 02 2020
accepted: 05 02 2020
pubmed: 3 3 2020
medline: 18 12 2020
entrez: 2 3 2020
Statut: ppublish

Résumé

Fibroblast growth factor receptor (FGFR)1 and FGFR4 have been associated with tumorigenesis in a variety of tumour types. As a therapeutic approach, their inhibition has been attempted in different types of malignancies, including lung cancer, and was initially focused on FGFR1-amplified tumours, though with limited success. In vitro and in vivo functional assessments of the oncogenic potential of downregulated/overexpressed genes in isogenic cell lines were performed, as well as inhibitor efficacy tests in vitro and in vivo in patient-derived xenografts (PDXs). mRNA was extracted from FFPE non-small cell lung cancer samples to determine the prognostic potential of the genes under study. We provide in vitro and in vivo evidence showing that expression of the adhesion molecule N-cadherin is key for the oncogenic role of FGFR1/4 in non-small cell lung cancer. According to this, assessment of the expression of genes in different lung cancer patient cohorts showed that FGFR1 or FGFR4 expression alone showed no prognostic potential, and that only co-expression of FGFR1 and/or FGFR4 with N-cadherin inferred a poorer outcome. Treatment of high-FGFR1 and/or FGFR4-expressing lung cancer cell lines and patient-derived xenografts with selective FGFR inhibitors showed high efficacy, but only in models with high FGFR1/4 and N-cadherin expression. Our data show that the determination of the expression of FGFR1 or FGFR4 alone is not sufficient to predict anti-FGFR therapy efficacy; complementary determination of N-cadherin expression may further optimise patient selection for this therapeutic strategy.

Sections du résumé

BACKGROUND BACKGROUND
Fibroblast growth factor receptor (FGFR)1 and FGFR4 have been associated with tumorigenesis in a variety of tumour types. As a therapeutic approach, their inhibition has been attempted in different types of malignancies, including lung cancer, and was initially focused on FGFR1-amplified tumours, though with limited success.
METHODS METHODS
In vitro and in vivo functional assessments of the oncogenic potential of downregulated/overexpressed genes in isogenic cell lines were performed, as well as inhibitor efficacy tests in vitro and in vivo in patient-derived xenografts (PDXs). mRNA was extracted from FFPE non-small cell lung cancer samples to determine the prognostic potential of the genes under study.
FINDINGS RESULTS
We provide in vitro and in vivo evidence showing that expression of the adhesion molecule N-cadherin is key for the oncogenic role of FGFR1/4 in non-small cell lung cancer. According to this, assessment of the expression of genes in different lung cancer patient cohorts showed that FGFR1 or FGFR4 expression alone showed no prognostic potential, and that only co-expression of FGFR1 and/or FGFR4 with N-cadherin inferred a poorer outcome. Treatment of high-FGFR1 and/or FGFR4-expressing lung cancer cell lines and patient-derived xenografts with selective FGFR inhibitors showed high efficacy, but only in models with high FGFR1/4 and N-cadherin expression.
INTERPRETATION CONCLUSIONS
Our data show that the determination of the expression of FGFR1 or FGFR4 alone is not sufficient to predict anti-FGFR therapy efficacy; complementary determination of N-cadherin expression may further optimise patient selection for this therapeutic strategy.

Identifiants

pubmed: 32114392
pii: S2352-3964(20)30058-X
doi: 10.1016/j.ebiom.2020.102683
pmc: PMC7047190
pii:
doi:

Substances chimiques

AZD4547 0
Antineoplastic Agents 0
Benzamides 0
Biomarkers, Tumor 0
Cadherins 0
Piperazines 0
Pyrazoles 0
FGFR1 protein, human EC 2.7.10.1
FGFR4 protein, human EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 1 EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 4 EC 2.7.10.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102683

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest Drs Quintanal-Villalonga, Molina-Pinelo, Carnero, Paz-Ares, and Ferrer jointly hold patent WO2019012174A1 and patent WO2019016422A1 (pending). Dr. Paz-Ares also reports personal fees from Roche, Lilly, MSD, BMS, AstraZeneca, Boehringer Ingelheim, Pfizer, Takeda, Novartis, Merck Serono, Amgen, Sanofi, Pharmamar, Clovis Oncology and Janssen outside the submitted work. JZ reports personal fees from Guardant Health. The remaining authors declare no conflict of interest.

Références

Cancer Res. 2015 Aug 1;75(15):3139-46
pubmed: 26048680
Clin Cancer Res. 2017 Sep 15;23(18):5527-5536
pubmed: 28630215
Traffic. 2005 Oct;6(10):947-54
pubmed: 16138907
Clin Cancer Res. 2012 Dec 15;18(24):6658-67
pubmed: 23082000
Proc Natl Acad Sci U S A. 2014 Oct 14;111(41):14788-93
pubmed: 25267614
Dis Markers. 2016;2016:9214056
pubmed: 27528792
Onco Targets Ther. 2015 May 22;8:1157-64
pubmed: 26045670
Cancer Discov. 2014 Feb;4(2):246-57
pubmed: 24302556
Phys Chem Chem Phys. 2017 Feb 1;19(5):3649-3659
pubmed: 28094372
PLoS One. 2014 Feb 11;9(2):e88032
pubmed: 24523874
J Clin Oncol. 2017 Jan 10;35(2):157-165
pubmed: 27870574
Cancer Res. 2007 Apr 1;67(7):3106-16
pubmed: 17409417
Wiley Interdiscip Rev Dev Biol. 2015 May-Jun;4(3):215-66
pubmed: 25772309
Oncogene. 2016 Jul 7;35(27):3587-97
pubmed: 26549034
Clin Cancer Res. 2014 Jun 15;20(12):3299-309
pubmed: 24771645
J Biol Chem. 2006 Nov 17;281(46):35208-16
pubmed: 17005551
Clin Cancer Res. 2017 Sep 15;23(18):5366-5373
pubmed: 28615371
Target Oncol. 2013 Mar;8(1):55-67
pubmed: 23325296
Oncogene. 2014 Jul 17;33(29):3776-83
pubmed: 24037524
Clin Cancer Res. 2012 Jul 15;18(14):3880-8
pubmed: 22573348
Mol Cancer Ther. 2015 Mar;14(3):704-12
pubmed: 25589496
Cancer. 2016 Oct;122(19):3024-31
pubmed: 27315356
Ann Oncol. 2017 Jun 1;28(6):1250-1259
pubmed: 28460066
Liver Int. 2014 Jul;34(6):e1-9
pubmed: 24393342
Biochim Biophys Acta. 2012 Apr;1823(4):850-60
pubmed: 22273505
Cancer Cell. 2002 Oct;2(4):301-14
pubmed: 12398894
Clin Cancer Res. 2012 May 1;18(9):2443-51
pubmed: 22407829
J Exp Clin Cancer Res. 2018 Aug 17;37(1):195
pubmed: 30119639
J Thorac Oncol. 2019 Apr;14(4):641-655
pubmed: 30639621
Nature. 2016 Jun 30;534(7609):647-51
pubmed: 27338794
Science. 2017 Jan 6;355(6320):84-88
pubmed: 28059768
Oncogene. 2012 Oct 11;31(41):4484-9
pubmed: 22158044
J Thorac Oncol. 2019 Jan;14(1):54-62
pubmed: 30267839
Clin Cancer Res. 2014 Dec 15;20(24):6551-8
pubmed: 25294908
Clin Lung Cancer. 2017 Nov;18(6):667-674.e1
pubmed: 28583379
Nat Commun. 2016 Jan 04;7:10262
pubmed: 26725515
Nat Cell Biol. 2001 Jul;3(7):650-7
pubmed: 11433297
CA Cancer J Clin. 2016 Jan-Feb;66(1):7-30
pubmed: 26742998
Sci Rep. 2018 Feb 5;8(1):2394
pubmed: 29402970
J Thorac Oncol. 2012 Dec;7(12):1775-1780
pubmed: 23154548
DNA Cell Biol. 2004 Sep;23(9):538-48
pubmed: 15383174
Ann Thorac Med. 2013 Oct;8(4):204-8
pubmed: 24250733
Oncol Rep. 2018 Jul;40(1):443-453
pubmed: 29750313
PLoS One. 2011;6(6):e20351
pubmed: 21666749
Virchows Arch. 2014 Nov;465(5):547-58
pubmed: 25086725
Lung Cancer. 2019 May;131:112-121
pubmed: 31027687
Oncogene. 2014 Jun 26;33(26):3411-21
pubmed: 23975425
J Mammary Gland Biol Neoplasia. 2010 Jun;15(2):117-34
pubmed: 20490631
Mol Cancer. 2013 Jul 31;12:83
pubmed: 23902722
Cancer Cell. 2012 Mar 20;21(3):448.e2
pubmed: 22439939
Int J Cancer. 1995 Apr 10;61(2):170-6
pubmed: 7705943
Oncotarget. 2017 Feb 28;8(9):16052-16074
pubmed: 28030802
Cancer Res. 2015 Oct 15;75(20):4398-406
pubmed: 26359452
Sci Transl Med. 2010 Dec 15;2(62):62ra93
pubmed: 21160078

Auteurs

Álvaro Quintanal-Villalonga (Á)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain; Molecular Pharmacology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Irene Ferrer (I)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain; CIBERONC, Madrid, Spain.

Elizabeth Guruceaga (E)

Bioinformatics Unit, Centre for Applied Medical Research (CIMA), Pamplona, Spain; PROTEORED, Madrid, Spain.

Cristina Cirauqui (C)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.

Ángela Marrugal (Á)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.

Laura Ojeda (L)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain; CIBERONC, Madrid, Spain.

Santiago García (S)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.

Jon Zugazagoitia (J)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain; CIBERONC, Madrid, Spain; Medical Oncology Department, Hospital Universitario Doce de Octubre. Madrid, Spain.

Sandra Muñoz-Galván (S)

CIBERONC, Madrid, Spain; Instituto de Biomedicina de Sevilla (IBIS) (HUVR, CSIC, Universidad de Sevilla), Sevilla, Spain.

Fernando Lopez-Rios (F)

CIBERONC, Madrid, Spain; Laboratorio de Dianas Terapéuticas, Hospital Universitario HM Sanchinarro, Madrid, Spain.

Luis Montuenga (L)

CIBERONC, Madrid, Spain; Program in Solid Tumors, Centre for Applied Medical Research (CIMA), Pamplona, Spain; Department of Pathology, Anatomy and Physiology, University of Navarra, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, SPAIN.

Silvestre Vicent (S)

CIBERONC, Madrid, Spain; Program in Solid Tumors, Centre for Applied Medical Research (CIMA), Pamplona, Spain; Department of Pathology, Anatomy and Physiology, University of Navarra, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, SPAIN.

Sonia Molina-Pinelo (S)

CIBERONC, Madrid, Spain; Instituto de Biomedicina de Sevilla (IBIS) (HUVR, CSIC, Universidad de Sevilla), Sevilla, Spain. Electronic address: smolina-ibis@us.es.

Amancio Carnero (A)

CIBERONC, Madrid, Spain; Instituto de Biomedicina de Sevilla (IBIS) (HUVR, CSIC, Universidad de Sevilla), Sevilla, Spain.

Luis Paz-Ares (L)

H12O-CNIO Lung Cancer Clinical Research Unit, Instituto de Investigación Hospital 12 de Octubre & Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain; CIBERONC, Madrid, Spain; Medical Oncology Department, Hospital Universitario Doce de Octubre. Madrid, Spain; Medical School, Universidad Complutense, Madrid, Spain.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH