Structure and Sequence of HumanFGF8

Gemel, Joanna; Gorry, Michael; Ehrlich, Garth D.; MacArthur, Craig A.

doi:10.1006/geno.1996.0349

Cited by 80 publications

(81 citation statements)

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“…This suggests that the RA-dependent loss of CAK phosphorylation of RARa induces FGF8 to regulate osteosarcoma cell differentiation. The human FGF8 gene encodes four alternatively spliced polypeptide products, including FGF8f, FGF8e, FGF8b and FGF8a (Gemel et al, 1996), the distinct functions of which in mediating cell differentiation remain unknown. By using different PCR primers specific for either total FGF8 mRNA or different FGF8 splice variants (Figure 7a), we first examined which FGF8 isoform(s) could be induced by RA and/or RARaS77A in U2OS cells.…”

Section: Ra-mediated Rara Hypophosphorylation Induces Fgf8f Expressionmentioning

confidence: 99%

“…FGF8f was induced with either RA treatment or RARaS77A expression (Figures 7b and c). Interestingly, FGF8 antibodies (sc-7916; Santa Cruz Biotechnology, Santa Cruz, CA, USA) only recognized a major 30-kDa protein, corresponding to the molecular mass of FGF8f (Gemel et al, 1996) on SDS-PAGE (Figure 7d), and Figure 4). RT-PCR analysis showed that FGF8f mimicked the RA effect of inducing expression of differentiation marker genes, including OPN, OPG, Runx2 and osteocalcin ( Figures 8c and d).…”

Section: Ra-mediated Rara Hypophosphorylation Induces Fgf8f Expressionmentioning

confidence: 99%

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Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

et al. 2010

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Section: Ra-mediated Rara Hypophosphorylation Induces Fgf8f Expressionmentioning

confidence: 99%

Section: Ra-mediated Rara Hypophosphorylation Induces Fgf8f Expressionmentioning

confidence: 99%

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

et al. 2010

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“…FGF 1, 2 and 3 have been detected in the cell nucleus (Cao et al, 1993;Presta et al, 1993;Antoine et al, 1997). Eight different splice variants of FGF8 are possible in the mouse but in man due to a stop codon only four of these forms are possible (Crossley and Martin, 1995;Gemel et al, 1996). Previous studies have indicated that FGF8b is the predominant form in breast tissue and that FGF8b has been shown to have the greatest transforming ability (MacArthur et al, 1995b).…”

Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 8 is expressed at higher levels in lactating human breast and in breast cancer

et al. 2002

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Fibroblast growth factor 8 can transform NIH3T3 cells and its expression has been found to be associated with breast and prostate cancer. Following our finding that fibroblast growth factor 8 mRNA expression is increased in breast cancer, we have undertaken an immunohistochemistry study of fibroblast growth factor 8 expression in a series of human breast tissues and other normal tissues. Our findings confirm increased expression of fibroblast growth factor 8 in malignant breast tissue but also show significant fibroblast growth factor 8 expression in non-malignant breast epithelial cells. No significant difference in fibroblast growth factor 8 expression was found between different grades of ductal carcinoma, lobular carcinoma and ductal carcinoma in-situ or cancer of different oestrogen receptor, progesterone receptor or nodal status. The highest levels of fibroblast growth factor 8 expression were found in lactating breast tissues and fibroblast growth factor 8 was also detected in human milk. A survey of other normal tissues showed that fibroblast growth factor 8 is expressed in the proliferative cells of the dermis and epithelial cells in colon, ovary fallopian tube and uterus. Fibroblast growth factor 8 appears to be expressed in several organs in man and appears to have an importance in lactation.

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“…Investigation on the involvement of FGF8b in hormone-related cancers was indeed based on the initial discovery of FGF8 (androgen-induced growth factor) in an androgen-dependent mouse mammary carcinoma cell line (Tanaka et al, 1992) and detection of FGF8 overexpression in human breast and prostate cancers (Tanaka et al, 1995;Leung et al, 1996;Gnanapragasam et al, 2002). Further genomic and functional characterization of the FGF8 family demonstrated that the FGF8b isoform (one of the four human FGF8 isoforms: FGF8a, b, e and f (Gemel et al, 1996)) possesses the greatest mitogenic and, more importantly, the greatest transforming activity than the other isoforms, both in vitro and in vivo (MacArthur et al, 1995a(MacArthur et al, , 1995bBlunt et al, 1997;Song et al, 2000;Olsen et al, 2006). It is believed that FGF8b is one of the most important FGF8 isoforms in human carcinogenesis Gnanapragasam et al, 2003), although the exact physiological function of each isoform is yet-to-be fully revealed.…”

Section: Introductionmentioning

confidence: 99%

FGF8b oncogene mediates proliferation and invasion of Epstein–Barr virus-associated nasopharyngeal carcinoma cells: implication for viral-mediated FGF8b upregulation

et al. 2010

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The fibroblast growth factor 8b (FGF8b) oncogene is known to be primarily involved in the tumorigenesis and progression of hormone-related cancers. Its role in other epithelial cancers has not been investigated, except for esophageal cancer, in which FGF8b overexpression was mainly found in tumor biopsies of male patients. These observations were consistent with previous findings in these cancer types that the male sex-hormone androgen is responsible for FGF8b expression. Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer of head and neck commonly found in Asia. It is etiologically associated with Epstein-Barr Virus (EBV) infection, inflammatory tumor microenvironment and relatively higher male predominance. Here, we reported for the first time that FGF8b is overexpressed in this EBV-associated non-hormone-related cancer of the head and neck, NPC. More importantly, overexpression of FGF8b mRNA and protein was detected in a large majority of NPC tumors from both male and female genders, in addition to multiple NPC cell lines. We hypothesized that FGF8b overexpression may contribute to NPC tumorigenesis. Using EBV-associated NPC cell lines, we demonstrated that specific knockdown of FGF8b by small interfering RNA inhibited cell proliferation, migration and invasion, whereas exogenous FGF8b stimulated these multiple phenotypes. Further mechanistic investigation revealed that in addition to NF-jB signaling (a major inflammatory signaling pathway known to be activated in NPC), an important EBV oncoprotein, the latent membrane protein 1 (LMP1), was found to be a direct inducer of FGF8b overexpression in NPC cells, whereas androgen (testosterone) has minimal effect on FGF8b expression in EBVassociated NPC cells. In summary, our study has identified LMP1 as the first viral oncogene capable of directly inducing FGF8b (an important cellular oncogene) expression in human cancer cells. This novel mechanism of viral-mediated FGF8 upregulation may implicate a new role of oncoviruses in human carcinogenesis.

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Structure and Sequence of HumanFGF8

Cited by 80 publications

References 1 publication

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

Fibroblast growth factor 8 is expressed at higher levels in lactating human breast and in breast cancer

FGF8b oncogene mediates proliferation and invasion of Epstein–Barr virus-associated nasopharyngeal carcinoma cells: implication for viral-mediated FGF8b upregulation

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