Structure and Expression of the Rat mRNA Encoding a Novel Member of the Fibroblast Growth Factor Family

Yamasaki, Masahiro; Miyake, Ayumi; Tagashira, Shuzou; Itoh, Nobuyuki

doi:10.1074/jbc.271.27.15918

Cited by 271 publications

(159 citation statements)

References 14 publications

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“…Fibroblast growth factor 2 (FGF-2) belongs to a family of heparin-binding polypeptides including 18 members which share 30 ± 60% amino acid identity (Ohbayashi et al, 1998;Jaye et al, 1986;Bikfalvi et al, 1997;Miyamoto et al, 1993;Yamasaki et al, 1996). Cell response to FGF-2 is mediated by a dual receptor system consisting of low and high a nity binding sites (Yayon et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Functional Rac-1 and Nck signaling networks are required for FGF-2-induced DNA synthesis in MCF-7 cells

Liu

Chevet

Kebache³

et al. 1999

Oncogene

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The e ects of Fibroblast Growth Factor-2 (FGF-2) on breast cancer cell DNA synthesis are controversial. To elucidate the mechanisms by which FGF-2 stimulates or inhibits DNA synthesis, we analysed FGF-2 signaling pathways in breast cancer MCF-7 and MCF-7 cells overexpressing Ha-Ras (MCF-7ras). We found that FGF-2-induction of DNA synthesis correlates with Ras transient activation, FRS-2 tyrosine phosphorylation and low level of expression of p66 Shc . In addition, Nckassociated proteins are highly tyrosine phosphorylated and JNK reaches a higher level of activation when FGF-2 triggers DNA synthesis. Interestingly upon FGF-2 treatment, JNK activation and DNA synthesis are dependent on Rac-1 activity. These results con®rm that in MCF-7 cells, induction of DNA synthesis by FGF-2 requires a transient activation of the Ras/MAPK cascade and demonstrates for the ®rst time that intact Rac-1 and Nck signaling networks are required.

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Section: Introductionmentioning

confidence: 99%

Functional Rac-1 and Nck signaling networks are required for FGF-2-induced DNA synthesis in MCF-7 cells

Liu

Chevet

Kebache³

et al. 1999

Oncogene

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“…FGFs are angiogenic and mitogenic, and have been implicated in a variety of human neoplasms (Basilico and Moscatelli, 1992;Burgess and Winkles, 1996). The FGF family consists presently of at least ten members, acidic FGF (aFGF or FGF-1), basic FGF (bFGF or FGF-2), FGF-3 (int-2), FGF-4 (hst/kFGF), FGF-5, FGF-6, keratinocyte growth factor (KGF or FGF-7), androgen-induced growth factor (AIGF or FGF-8), glia-activating factor , and FGF-10 (Yamasaki et al, 1996). The FGF-5 gene, located on chromosome 4q11 (Nguyen et al, 1988), was originally discovered as a human oncogene which had acquired transforming potential by DNA rearrangement accompanying transfection of NIH3T3 cells with human tumor DNA (Zhan et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor-5 stimulates mitogenic signaling and is overexpressed in human pancreatic cancer: evidence for autocrine and paracrine actions

et al. 1997

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Fibroblast growth factor (FGF)-1 and -2 are overexpressed in human pancreatic cancer. 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. 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. Densitometric analysis indicated that 4.0 kb and 1.6 kb FGF-5 mRNA transcripts levels were increased 2.4-and 2.7-fold in the cancers by comparison with normal tissues, respectively (P50.002, P50.0001). Immunohistochemistry and in situ hybridization demonstrated that FGF-5 localized in the cancer cells, stromal ®broblast and in¯itrating macrophages. FGF-5 mRNA was also detected in COLO-357 human pancreatic cancer cells. Furthermore, secreted FGF-5 protein was present in conditioned medium of COLO-357 cells. Exogeneous FGF-5 (0.37 nM) increased the growth of COLO-357 cells by 48% (P50.0001) and increased mitogenactivated protein kinase activity. COLO-357 cells expressed the IIIc isoform of the type I FGF receptor, the preferred FGF receptor for FGF-5. These observations suggest that FGF-5 may participate in autocrine and paracrine pathways promoting pancreatic cancer cell growth in vivo.

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“…As it stands now, the FGF family comprises 10 characterized growth regulatory proteins that share 35 ± 50% overall homology (reviews in Basilico and Moscatelli, 1992;Goldfarb, 1996, and for FGF-10: Yamasaki et al, 1996). FGF-3 to 8 and FGF-10 are each synthesized with a signal peptide which transports them to the secretory pathway, whereas FGF-1, -2 and -9 which lack a signal peptide, are released from the cells by unknown mechanisms.…”

Section: Introductionmentioning

confidence: 99%

FGF-3 and FGF-4 elicit distinct oncogenic properties in mouse mammary myoepithelial cells

et al. 1998

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Fibroblast Growth Factors 3 (FGF-3) and 4 (FGF-4) were compared for the e ects they each exert on EF43 mouse cells. This non-transformed mammary cell line appears to be myoepithelial mainly because it expresses a-smooth muscle actin. The EF43 cells were infected with similar vectors that carry either the short fgf-3 sequence (the product of which goes into the secretory pathway), fgf-4 or the selection gene only as control. In syngeneic animals, EF43.fgf-3 cells were tumorigenic only when orthotopically implanted whereas EF43.fgf-4 cells invariably gave rise to aggressive tumors. However, both tumor types were metastatic as evidenced by the blue micrometastases observed when the implanted cells expressed lacZ. In vitro, the FGF-3 producing cells were strongly invasive in matrigel coated chambers whereas the EF43.fgf-4 cells only were invasive in type I-collagen gels. Interestingly, FGF-3 production greatly stimulated the synthesis of pro-MMP-9 (Matrix Metalloprotease-9) and, to a lesser extent, that of pro-MMP-2. FGF-3 also up-regulated the production of plasminogen activators. In contrast, FGF-4 had no e ect on these secretions and the medium conditioned by the EF43.fgf-4 cells displayed the largest plasminogen activator ± inhibitor activity. These results show that FGF-3 and FGF-4 have distinct mechanisms of action on myoepithelial cells.

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Structure and Expression of the Rat mRNA Encoding a Novel Member of the Fibroblast Growth Factor Family

Cited by 271 publications

References 14 publications

Functional Rac-1 and Nck signaling networks are required for FGF-2-induced DNA synthesis in MCF-7 cells

Functional Rac-1 and Nck signaling networks are required for FGF-2-induced DNA synthesis in MCF-7 cells

Fibroblast growth factor-5 stimulates mitogenic signaling and is overexpressed in human pancreatic cancer: evidence for autocrine and paracrine actions

FGF-3 and FGF-4 elicit distinct oncogenic properties in mouse mammary myoepithelial cells

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