Disease relevance of FGF5

• The mRNAs for the other four members of the fibroblast growth factor (FGF) family, including acidic FGF, int-2 protein, hst-1 protein, FGF5 protein and FGF6/hst-2 protein could not be detected in the esophageal and gastric cancer cell lines [1].
• In this study, the expression of FGF5 was explored in choroidal neovascular membranes removed from patients with age-related macular degeneration (ARMD) [2].
• FGF-5 mRNA was also detected in COLO-357 human pancreatic cancer cells [3].
• Furthermore, they demonstrate a contrasting expression pattern of FGF5 and FGFB genes, both involved in the growth factor pathogenic cascade leading to Kaposi's sarcoma [4].
• FGF5 gene expression was detected in the characteristic Kaposi's sarcoma spindle-shaped cells in the five samples from human immunodeficiency-positive (HIV+) patients [4].

High impact information on FGF5

• In a model of stress-induced myocardial ischemia, intracoronary injection of a recombinant adenovirus expressing human fibroblast growth factor-5 (FGF-5) resulted in messenger RNA and protein expression of the transferred gene [5].
• Northern analysis of total RNA from rat skeletal muscle revealed an FGF-5 mRNA transcript both during the period of embryonic motoneuron death and in the adult [6].
• Hair follicles from PG and DeltaN80PG mice show premature termination of the growth phase (anagen) of the hair cycle, an event that is regulated in part by FGF5 (Hebert et al. 1994) [7].
• The BEK receptor expressed in Chinese hamster ovary cells binds acidic FGF, basic FGF, and Kaposi FGF equally well but does not bind keratinocyte growth factor or FGF-5 appreciably [8].
• The introduction of these ORF-1 mutations into a eukaryotic FGF-5 expression vector increases its capacity to transform mouse NIH 3T3 cells up to 50-fold upon transfection [9].

Chemical compound and disease context of FGF5

• Biopsy samples from five acquired immune deficiency syndrome (AIDS)-Kaposi's sarcomas and one non-AIDS-associated Kaposi's sarcoma were assayed by in situ RNA hybridization onto paraformaldehyde-fixed, paraffin-embedded skin sections for the presence of two fibroblast growth factor gene transcripts, FGFB and FGF5 [4].
• C2 CTLs, cloned from human CTLs infiltrating a renal cell carcinoma, kill cancer cells overexpressing fibroblast growth factor-5 (FGF-5) [10].

Biological context of FGF5

• The membranes were immunostained with an affinity purified rabbit polyclonal antibody raised against the amino acid sequence for residues 175 to 185 of human FGF5 and visualized with the silver enhanced colloidal gold method for light microscopy [2].
• In our study, we show a synteny between EGF and the genes PDHA2 and FGF5 (from HSA 4q) and microsatellites ILSTS018, ILSTS090, and ILSTS093 (from bovine chromosome 6) in sheep [11].
• These observations suggest that FGF-5 may participate in autocrine and paracrine pathways promoting pancreatic cancer cell growth in vivo [3].
• To elucidate the inherent participation of FGF5 during limb organogenesis, a retroviral delivery system (RCAS) was used to overexpress human FGF5 throughout developing hind limb of chicken embryos [12].
• We now term this oncogene the FGF-5 gene, since it specifies the fifth documented protein related to fibroblast growth factors (FGFs [13].

Anatomical context of FGF5

• Use of the ARPE-19 cell line as a model of RPE polarity: basolateral secretion of FGF5 [14].
• RESULTS: FGF5 was expressed in membranes arising from ARMD, and was found primarily in blood vessels and the surrounding extracellular matrix [2].
• Expression of FGF5 in choroidal neovascular membranes associated with ARMD [2].
• In PC12 cells, expression of hFGF-5 or exposure to hFGF-5 protein induced differentiation [15].
• Immunohistochemistry and in situ hybridization demonstrated that FGF-5 localized in the cancer cells, stromal fibroblast and inflitrating macrophages [3].

Associations of FGF5 with chemical compounds

• Although both of these agents which are FGF binding antagonists were found to inhibit the incorporation of 3H thymidine in KS-derived cultured cells, increased expression of bFGF, FGF5 and the FGF receptor was observed after the KS cells were exposed to these substances [16].
• FGF-5 is secreted from transfected 3T3 cells and from human tumor cells as glycoproteins containing heterogeneous amounts of sialic acid [9].
• Expression of the IIIc variant of FGF receptor-1 confers mitogenic responsiveness to heparin and FGF-5 in TAKA-1 pancreatic ductal cells [17].
• Here we show that C2 cells recognize human leukocyte antigen-A3 MHC class I molecules presenting a nine-residue FGF-5 peptide generated by protein splicing [10].

Other interactions of FGF5

• METHODS: Influenza infection and adenovirus-mediated gene transfer were used to deliver and express genes encoding influenza hemagglutinin (HA), p75-NTR (a neurotrophin receptor), low-density lipoprotein (LDL) receptor (LDLR), and FGF5 in confluent monolayers of ARPE-19 cells [14].
• COLO-357 cells expressed the IIIc isoform of the type I FGF receptor, the preferred FGF receptor for FGF-5 [3].
• In this study the role of FGF-5 in human pancreatic cancer was investigated, as FGF-5 has a classical signal sequence for secretion not found in FGF-1 or -2 [3].
• Exogeneous FGF-5 (0.37 nM) increased the growth of COLO-357 cells by 48% (P < 0.0001) and increased mitogen-activated protein kinase activity [3].
• Additional mRNA transcripts encoding FGF-5 and FGF-7 were expressed by RA, but not normal, synovial cells in culture [18].

Analytical, diagnostic and therapeutic context of FGF5

• Northern blot analysis with a 306 bp FGF-5 cDNA revealed the presence of 4.0 kb and 1.6 kb FGF-5 mRNA transcripts in both normal and cancerous pancreatic tissues [3].
• Acidic FGF (aFGF) and FGF-5 were detected in two of six and four of six KS tumor specimens, respectively, whereas both of these growth factors were expressed in all of the cell cultures, including six KS-derived cell cultures and human endothelial cells and smooth muscle cells [19].
• FGF-5 expression by quantitative real-time reverse transcription PCR in normal tissues was below the recognition threshold for this CTL [20].
• As a normal protein with significant overexpression by multiple adenocarcinomas and little normal tissue expression, FGF-5 represents an immunotherapy target with potential utility against a broad array of nonmelanoma cancers [20].
• Significant rescue from photoreceptor cell death was found after injections of vectors expressing either FGF-5 or FGF-18 in the animal models [21].

References