Anti-FGF3: Polyclonal Fibroblast Growth Factor 3 Antibody

BACKGROUND FGFs comprise a large family of proteins that includes at least 22 known members. FGFs bind and signal through low and high affinity FGF receptors. The four known high affinity receptors (FGFR1–4) are structurally similar transmembrane receptor tyrosine kinases. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion.¹

FGF3 belongs to the FGF7 subfamily together with FGF7, FGF10 and FGF22. Only FGF3 and FGF10 have been implicated in pituitary function, particularly during embryonic development. FGF3 is expressed in de ventral diencephalon bordering Rathke’s pouch during early embryonic development. FGF3 has a distinct pattern of expression throughout development in vertebrates. In the mouse embryo, FGF3 transcripts were detected in the rhombencephalon at a developmental stage when the induction of the inner ear occurs.² It was shown that FGF3 constitutes a signal for the induction of the otic vesicle, the primordium of the inner ear: the formation of the otic vesicle was inhibited by antisense oligonucleotides targeted to the secreted form of FGF3, and by antibodies against FGF3 oncoproteins; and basic FGF can mimic the inductive signal in the absence of the rhombencephalon. Congenital deafness due to mutation in the FGF3 gene could be sought by identifying a form of deafness that maps to 11q. The neuroendocrine role of FGF3 has been mainly studied in zebrafish. Paracrine FGF3 signaling from the ventral diencephalon is required to induce the expression of several pituitary-specific genes, such as lim3, pit1 and others in the pituitary progenitor cells. FGF3 null mutants do not express the latter genes. However, initially they form a pituitary anlage of normal size and shape but subsequently all the pituitary cells die by apoptosis. Interestingly, graded attenuation of FGF3 signalling either by FGF3 morpholino treatment or by treatment of embryos with the FGF receptor inhibitor at graded doses show diminished POMC cell migration and development in the pituitary intermediate lobe at the lower doses while development in the anterior lobe remains normal. Also other anterior lobe endocrine cells develop normally at the lower inhibitor doses. In addition, using immunohistochemistry with a tissue microarray containing nonsmall cell lung cancer samples, it was demonstrated that overexpression of FGF3 and EGFR in 61% and 69% of samples, respectively. They found significant correlation (p less than 0.001) between overexpression of EGFR and of FGF3. It was suggested that co-overexpression of EGFR and FGF3 may play an important role in the pathogenesis of lung carcinoma.³ Furthermore, frequent amplification of FGF3 gene has been found in human tumors, which may be important for neoplastic transformation and tumor progression.

 

REFERENCES  

1. Turner, N. & Grose, R.: Nat. Rev. Cancer 10:116-29, 2010
2. Represa, J. et al: Nature 353:561-3,1991
3. Tai, A.L. et al: Cancer 106:146-55, 2006