Nuclear action of FGF members in endocrine-related tissues and cancer: Interplay with steroid receptor pathways

Dysregulation of the fibroblast growth factors/fibroblast growth factor receptor (FGF/FGFR) pathway has been implicated in a wide range of human disorders and several members have been localized in the nuclear compartment. Hormone-activated steroid receptors or ligand independent activated receptors...

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Bibliographic Details
Published in:Steroids 2019-12, Vol.152, p.108492-108492, Article 108492
Main Authors: Figueroa, Virginia, Rodríguez, María Sol, Lanari, Claudia, Lamb, Caroline Ana
Format: Article
Language:English
Subjects:
Animals
Breast cancer
Cell Nucleus - metabolism
Endocrine resistance
Endocrine System - metabolism
Endocrine-related tissues and cancer
FGF/FGFR axis
Fibroblast Growth Factors - genetics
Fibroblast Growth Factors - metabolism
Humans
Neoplasms - metabolism
Nuclear FGF/FGFR
Receptors, Steroid - metabolism
Steroid receptor pathway
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Summary:Dysregulation of the fibroblast growth factors/fibroblast growth factor receptor (FGF/FGFR) pathway has been implicated in a wide range of human disorders and several members have been localized in the nuclear compartment. Hormone-activated steroid receptors or ligand independent activated receptors form nuclear complexes that activate gene transcription. This review aims to highlight the interplay between the steroid receptor and the FGF/FGFR pathways and focuses on the current knowledge on nuclear action of FGF members in endocrine-related tissues and cancer. The nuclear trafficking and targets of FGF/FGFR members and the available evidence on the interplay with steroid hormones and receptors is described. Finally, the data on aberrant FGF/FGFR signaling is summarized and the nuclear action of FGF members on endocrine resistant breast cancer is highlighted. Identifying the mechanisms underlying FGF-induced endocrine resistance will be important to understand how to efficiently target endocrine-related diseases and even enhance or restore endocrine sensitivity in hormone receptor positive tumors.
ISSN:0039-128X
1878-5867
DOI:10.1016/j.steroids.2019.108492