Molecular Signatures for Combined Targeted Treatments in Diffuse Malignant Peritoneal Mesothelioma.
Adult
Aged
Cell Line, Tumor
Combined Modality Therapy
/ methods
Down-Regulation
/ drug effects
Female
Humans
Lung Neoplasms
/ drug therapy
Male
Mesothelioma
/ drug therapy
Mesothelioma, Malignant
MicroRNAs
/ genetics
Middle Aged
Neoplasm Recurrence, Local
/ genetics
Peritoneal Neoplasms
/ drug therapy
Peritoneum
/ drug effects
Protein Kinase Inhibitors
/ therapeutic use
RNA, Messenger
/ genetics
Axl
EGFR family
MET
diffuse malignant peritoneal mesothelioma
mTOR/PIK3
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
19 Nov 2019
19 Nov 2019
Historique:
received:
20
09
2019
revised:
08
11
2019
accepted:
15
11
2019
entrez:
23
11
2019
pubmed:
23
11
2019
medline:
9
4
2020
Statut:
epublish
Résumé
Background-There are currently no effective therapies for diffuse malignant peritoneal mesothelioma (DMPM) patients with disease recurrence. In this study, we investigated the biology of DMPM by analyzing the EGFR family, Axl, and MET, in order to assess the presence of cross-talk between these receptors, suggesting the effectiveness of combined targeted treatments in DMPM. Method-We analyzed a series of 22 naïve epithelioid DMPM samples from a single institute, two of which showed higher-grade malignancy ("progressed"). EGFR, HER2, HER3, Axl, and MET activation and expression were investigated by biochemical analysis, real-time PCR immunofluorescence, immunohistochemistry, next-generation sequencing, miRNA, and mRNA in situ hybridization. Results-In most DMPMs, a strong EGFR activation was associated with HER2, HER3, Axl, and MET co-activation, mediated mainly by receptor heterodimerization and autocrine-paracrine loops induced by the expression of their cognate ligands. Axl expression was downregulated by miRNA34a. Mutations in MET Sema domain were exclusively found in two "progressed" DMPMs, and the combined Axl and MET inhibition reduced cellular motility in a DMPM cell line obtained from a "progressed" DMPM. Conclusion-The results indicate that the coordinated activity of multiple cross-talks between RTKs is directly involved in the biology of DMPM, suggesting the combined inhibition of PIK3 and mTOR as an effective strategy that may be easily implemented in clinical practice, and indicating that the combined inhibition of EGFR/HER2 and HER3 and of Axl and MET deserves further investigation.
Identifiants
pubmed: 31752449
pii: ijms20225817
doi: 10.3390/ijms20225817
pmc: PMC6888071
pii:
doi:
Substances chimiques
MicroRNAs
0
Protein Kinase Inhibitors
0
RNA, Messenger
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Ministero della Salute, Ricerca Finalizzata 2009 (RF-2009-1546664, MD)
ID : RF-2009-1546664
Références
J Thorac Oncol. 2011 May;6(5):864-74
pubmed: 21774103
Cancer. 2011 Jan 15;117(2):361-71
pubmed: 20839315
Nat Med. 2009 Sep;15(9):1010-2
pubmed: 19734877
Br J Cancer. 2014 May 13;110(10):2479-88
pubmed: 24762959
Sci Signal. 2017 Jan 03;10(460):
pubmed: 28049763
Cancer Metastasis Rev. 2012 Feb 3;:
pubmed: 22302111
J Thorac Oncol. 2015 Feb;10(2):387-91
pubmed: 25611229
Nat Genet. 2012 Jul 01;44(8):852-60
pubmed: 22751098
Lung Cancer. 2009 May;64(2):211-8
pubmed: 19042053
JAMA Oncol. 2018 Feb 1;4(2):235-238
pubmed: 28910456
Mod Pathol. 2017 Feb;30(2):246-254
pubmed: 27813512
Clin Cancer Res. 2005 Mar 15;11(6):2300-4
pubmed: 15788680
Oncotarget. 2016 Nov 15;7(46):75503-75517
pubmed: 27705913
Ann Oncol. 2010 Feb;21(2):348-53
pubmed: 19635740
J Clin Oncol. 2007 Jun 10;25(17):2406-13
pubmed: 17557954
Hum Mutat. 2018 Mar;39(3):371-377
pubmed: 29219214
Cell. 2008 May 16;133(4):704-15
pubmed: 18485877
Oncol Rep. 2012 Jun;27(6):1794-800
pubmed: 22426987
Int J Mol Sci. 2019 Feb 16;20(4):
pubmed: 30781524
Oncogene. 2014 Mar 6;33(10):1316-24
pubmed: 23474758
Ann Surg Oncol. 2015 May;22(5):1686-93
pubmed: 25124472
Oncogene. 2014 Aug 7;33(32):4185-92
pubmed: 24056961
Oncogene. 2016 Feb 18;35(7):878-86
pubmed: 25961915
Cancer Res. 2009 Sep 1;69(17):6871-8
pubmed: 19671800
Eur J Cancer. 2013 Oct;49(15):3140-8
pubmed: 23831335
Genome Med. 2019 Feb 18;11(1):8
pubmed: 30777124
Ann Surg Oncol. 2018 Aug;25(8):2159-2164
pubmed: 29423664
J Hematol Oncol. 2017 Jan 18;10(1):19
pubmed: 28100259
Eur J Cancer. 2010 Oct;46(15):2837-48
pubmed: 20692828
Oncol Rep. 2017 Apr;37(4):2201-2208
pubmed: 28260071
J Clin Pathol. 2015 Aug;68(8):661-4
pubmed: 25934842
ESMO Open. 2017 Apr 12;2(1):e000101
pubmed: 28761723
Clin Cancer Res. 2016 Jun 15;22(12):2874-84
pubmed: 26787751
Oncogene. 2010 Sep 23;29(38):5254-64
pubmed: 20603615
Neoplasia. 2011 Jan;13(1):12-22
pubmed: 21245936
Brief Bioinform. 2013 Mar;14(2):178-92
pubmed: 22517427
Oncogene. 2011 Jun 23;30(25):2888-99
pubmed: 21317930