Publication: Fibroblast growth factor receptors: multifactorial-contributors to tumor initiation and progression
Authors
Feng, Shachuan ; Zhou, Li ; Collins Nice, Edouard ; Huang, Canhua
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-30.13
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info:eu-repo/semantics/article
Description
Abstract
Fibroblast growth factor receptors (FGFRs),
encoded by four genes (FGFR1, FGFR2, FGFR3, and
FGFR4) are tightly associated with many biological
processes such as organ development, cell proliferation
and migration. Studies over the past decades have
validated the pivotal roles FGFRs play in tumorigenesis
due to the regulation of diverse tumorigenesis-related
processes, including cell survival, proliferation,
inflammation, metastasis and angiogenesis. Interestingly,
FGFR mutations in somatic cells leading to
tumorigenesis and those in germ cells leading to
developmental disorders are identical, suggesting that
FGFR mutations result in different diseases due to their
spatio-temporal expression. Thus, discoveries in
developmental biology may also be applicable to cancer.
FGFRs regulate the expression and/or the activity of a
myriad of molecules (e.g. matrix metalloproteinases
(MMPs) and Snail) that are tightly linked to
tumorigenesis by four main signaling pathways (RASMAPK, PI3K-AKT, PLCγ-PIP2, and STAT), as well as
other minor branches. Epigenetic and genetic alteration
of FGFR genes, including DNA methylation, histone
remodeling, microRNA regulation, single nucleotide
polymorphisms (SNPs), gene missense mutations,
amplification, and fusion of FGFRs with other genes,
which result in gain or loss of FGFR function, have been
identified in many types of cancer. In this review, we
focus in particular on recent advances in the relationship
between FGFR disorders and tumorigenesis.
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Citation
Histology and Histopathology, Vol. 30, n.º 1 (2015)
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Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/