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FGFR3-TACC3 is an oncogenic fusion protein in respiratory epithelium

Oncogene, 2018-11, Vol.37 (46), p.6096-6104 [Peer Reviewed Journal]

COPYRIGHT 2018 Nature Publishing Group ;Copyright Nature Publishing Group Nov 2018 ;ISSN: 0950-9232 ;EISSN: 1476-5594 ;DOI: 10.1038/s41388-018-0399-5 ;PMID: 29991799

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Title:
FGFR3-TACC3 is an oncogenic fusion protein in respiratory epithelium
Author: Best, Sarah A ; Harapas, Cassandra R ; Kersbergen, Ariena ; Rathi, Vivek ; Asselin-Labat, Marie-Liesse ; Sutherland, Kate D
Subjects: Adenocarcinoma of Lung - genetics ; Animal genetic engineering ; Animals ; Cancer ; Carcinoma, Non-Small-Cell Lung - genetics ; Care and treatment ; Cell Line, Tumor ; Cre recombinase ; Development and progression ; Epithelial cells ; Epithelium ; Fibroblast growth factor receptor 3 ; Fibroblast growth factor receptors ; Fibroblast growth factors ; Fusion protein ; Gene expression ; Genes ; Genetic aspects ; Genetic engineering ; Genetic transformation ; Genomes ; Genomics ; Health aspects ; Humans ; Lung - metabolism ; Lung cancer ; Lung Neoplasms - genetics ; Lung tumors ; Lungs ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins - genetics ; Non-small cell lung cancer ; Non-small cell lung carcinoma ; Nose ; Olfactory epithelium ; Oncogene Proteins, Fusion - genetics ; p53 Protein ; Receptor, Fibroblast Growth Factor, Type 3 - genetics ; Recombination ; Respiratory Mucosa - metabolism ; Respiratory tract ; Rodents ; Small cell lung cancer ; Stem cell research ; Transgenic mice ; Tumor proteins ; Tumor suppressor genes ; Tumorigenesis ; Tumors
Is Part Of: Oncogene, 2018-11, Vol.37 (46), p.6096-6104
Description: Structural rearrangements of the genome can drive lung tumorigenesis through the generation of fusion genes with oncogenic properties. Advanced genomic approaches have identified the presence of a genetic fusion between fibroblast growth factor receptor 3 (FGFR3) and transforming acidic coiled-coil 3 (TACC3) in non-small cell lung cancer (NSCLC), providing a novel target for FGFR inhibition. To interrogate the functional consequences of the FGFR3-TACC3 fusion in the transformation of lung epithelial cells, we generated a novel transgenic mouse model that expresses FGFR3-TACC3 concomitant with loss of the p53 tumor suppressor gene. Intranasal delivery of an Ad5-CMV-Cre virus promoted seromucinous glandular transformation of olfactory cells lining the nasal cavities of FGFR3-TACC3 (LSL-F3T3) mice, which was further accelerated upon loss of p53 (LSL-F3T3/p53). Surprisingly, lung tumors failed to develop in intranasally infected LSL-F3T3 and LSL-F3T3/p53 mice. In line with these observations, we demonstrated that intranasal delivery of Ad5-CMV-Cre induces widespread Cre-mediated recombination in the olfactory epithelium. Intra-tracheal delivery of Ad5-CMV-Cre into the lungs of LSL-F3T3 and LSL-F3T3/p53 mice, however, resulted in the development of lung adenocarcinomas. Taken together, these findings provide in vivo evidence for an oncogenic function of FGFR3-TACC3 in respiratory epithelium.
Publisher: England: Nature Publishing Group
Language: English
Identifier: ISSN: 0950-9232
EISSN: 1476-5594
DOI: 10.1038/s41388-018-0399-5
PMID: 29991799
Source: MEDLINE
Alma/SFX Local Collection
ProQuest Central

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FGFR3-TACC3 is an oncogenic fusion protein in respiratory epithelium

COPYRIGHT 2018 Nature Publishing Group ;Copyright Nature Publishing Group Nov 2018 ;ISSN: 0950-9232 ;EISSN: 1476-5594 ;DOI: 10.1038/s41388-018-0399-5 ;PMID: 29991799

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