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Oncogenic FGFR Fusions Produce Centrosome and Cilia Defects by Ectopic Signaling

A. Nita, SP. Abraham, P. Krejci, M. Bosakova

. 2021 ; 10 (6) : . [pub] 20210609

Jazyk angličtina Země Švýcarsko

Typ dokumentu časopisecké články, práce podpořená grantem, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/bmc22004220

Grantová podpora
LTAUSA19030 Ministry of Education, Youth and Sports of the Czech Republic

A single primary cilium projects from most vertebrate cells to guide cell fate decisions. A growing list of signaling molecules is found to function through cilia and control ciliogenesis, including the fibroblast growth factor receptors (FGFR). Aberrant FGFR activity produces abnormal cilia with deregulated signaling, which contributes to pathogenesis of the FGFR-mediated genetic disorders. FGFR lesions are also found in cancer, raising a possibility of cilia involvement in the neoplastic transformation and tumor progression. Here, we focus on FGFR gene fusions, and discuss the possible mechanisms by which they function as oncogenic drivers. We show that a substantial portion of the FGFR fusion partners are proteins associated with the centrosome cycle, including organization of the mitotic spindle and ciliogenesis. The functions of centrosome proteins are often lost with the gene fusion, leading to haploinsufficiency that induces cilia loss and deregulated cell division. We speculate that this complements the ectopic FGFR activity and drives the FGFR fusion cancers.

Citace poskytuje Crossref.org

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$a A single primary cilium projects from most vertebrate cells to guide cell fate decisions. A growing list of signaling molecules is found to function through cilia and control ciliogenesis, including the fibroblast growth factor receptors (FGFR). Aberrant FGFR activity produces abnormal cilia with deregulated signaling, which contributes to pathogenesis of the FGFR-mediated genetic disorders. FGFR lesions are also found in cancer, raising a possibility of cilia involvement in the neoplastic transformation and tumor progression. Here, we focus on FGFR gene fusions, and discuss the possible mechanisms by which they function as oncogenic drivers. We show that a substantial portion of the FGFR fusion partners are proteins associated with the centrosome cycle, including organization of the mitotic spindle and ciliogenesis. The functions of centrosome proteins are often lost with the gene fusion, leading to haploinsufficiency that induces cilia loss and deregulated cell division. We speculate that this complements the ectopic FGFR activity and drives the FGFR fusion cancers.
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$a Abraham, Sara P $u Department of Biology, Faculty of Medicine, Masaryk University, 62500 Brno, Czech Republic
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$a Krejci, Pavel $u Department of Biology, Faculty of Medicine, Masaryk University, 62500 Brno, Czech Republic $u Institute of Animal Physiology and Genetics of the CAS, 60200 Brno, Czech Republic $u International Clinical Research Center, St. Anne's University Hospital, 65691 Brno, Czech Republic
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