FGF-2 and FGF-1 expressed in rat bladder carcinoma cells have similar angiogenic potential but different tumorigenic properties in vivo

Jouanneau, Jacqueline; Plouët, Jean; Moens, G; Thiery, Jean Paul

doi:10.1038/sj.onc.1200883

Cited by 41 publications

(31 citation statements)

References 22 publications

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“…In the rat bladder carcinoma NBT-II cell experimental model, the production of low molecular weight (18 kD) FGF-2 induces angiogenic tumors, but does not result in high level of tumorigenicity (Jouanneau et al, 1997). In contrast we show herein that production of the 24 kD FGF-2 alone results in NBT-II cells becoming tumorigenic and lung metastatic.…”

Section: Introductioncontrasting

confidence: 37%

“…G418-resistant clones were selected for the production of 24 kD FGF-2, and FGF-2 mRNA was detected by Northern blot analysis (data not shown). Most, but not all, of the transfected cells were epithelial-like in morphology, similar to parental NBT-II cells and 18 kD FGF-2-producing bGF22 cells (Jouanneau et al, 1997). Three clones, NLS20 (epithelial), NLS35 (epithelial) and NLS42 (®broblast-like) were chosen for further study.…”

Section: Expression Of 24 Kd Fgf-2mentioning

confidence: 99%

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Nuclear 24 kD fibroblast growth factor (FGF)-2 confers metastatic properties on rat bladder carcinoma cells

et al. 1999

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The tumorigenic and metastatic properties of rat bladder carcinoma NBT-II cells transfected with a cDNA encoding the 24 kD nuclear isoform of human ®broblast growth factor-2 (FGF-2) were analysed and compared with those cells producing the 18 kD cytoplasmic isoform FGF-2. In transfected clones, 24 kD FGF-2 was found in the nucleus, and no FGF-2 was secreted. RT ± PCR analysis showed no upregulation of FGF-2-speci®c receptor FGFR2c expression in these proliferating transfected cells. A shorter latency period for in vivo tumor formation and abundant spontaneous lung metastases were only seen if nuclear FGF-2-producing cells were injected subcutaneously into nude mice. Intravenous injection of 24 kD FGF-2-producing cells led to extensive experimental lung metastases whereas injection of control NBT-II cells or 18 kD FGF-2-producing cells did not. As FGF-2-producing cells have no speci®c FGF-2 receptors, our results suggest that the 24 kD FGF-2 has nuclear targets, and activates metastatic property of carcinoma cells via a mechanism other than the conventional FGF receptor-mediated signaling pathway.

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Section: Introductioncontrasting

confidence: 37%

Section: Expression Of 24 Kd Fgf-2mentioning

confidence: 99%

Nuclear 24 kD fibroblast growth factor (FGF)-2 confers metastatic properties on rat bladder carcinoma cells

et al. 1999

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“…53 FGF-1 has been found to induce a dysfunctional state of E-cadherin in a rat bladder cell line 54 and to confer a growth advantage to NET-II cells. 55,56 However, these effects are most probably cell type-and tissue-specific. For instance in an FGF-2 negative rat pancreatic cancer cell line, introduction of the FGF-2 gene leads to a dramatic reduction of tumour growth in nude mice.…”

Section: Discussionmentioning

confidence: 99%

FGF-1 and FGF-2 regulate the expression of E-cadherin and catenins in pancreatic adenocarcinoma

El‐Hariry¹,

Pignatelli

Lemoine

2001

Int. J. Cancer

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E-cadherin is a transmembrane protein that mediates Ca 2؉ -dependent cell-cell adhesion and is implicated in a number of biologic processes, including cell growth and differentiation, cell recognition and cell sorting during development. We have previously demonstrated that both cell-cell adhesion and invasion are modulated by fibroblast growth factor (FGF)-1 and FGF-2 in a panel of pancreatic adenocarcinoma cell lines (BxPc3, T3M4 and HPAF). Here, we examine further the role of FGFs in the expression and activation of the E-cadherin/catenin system. We demonstrate that both FGF-1 and FGF-2 upregulate E-cadherin and ␤-catenin at the protein level in the BxPc3 and HPAF cell lines and modestly in T3M4 cells. FGF-1 and FGF-2 facilitate the association of E-cadherin and ␣-catenin with the cytoskeleton, as demonstrated by the increase in the detergent-insoluble fraction of E-cadherin in BxPc3 and HPAF cells. Since the correct function of the E-cadherin/catenin complex requires its association with the cytoskeleton, our data suggest that FGF-1 and FGF-2 contribute to the integrity and thus the function of the complex. Furthermore, FGFs facilitate the assembly of the E-cadherin/catenin axis. The effect is associated with elevation of tyrosine phosphorylation of E-cadherin, ␣-catenin, ␤-4051catenin and ␥-catenin, but not p120 ctn . These findings indicate that the E-cadherin/catenin system is a target of the FGF/FGFR system and that coordinated signals from both systems may determine the ultimate biologic responses. © 2001 Wiley-Liss, Inc. Key words: E-cadherin; catenins; FGF; FGFR; pancreatic adenocarcinomaEvidence is compelling that a loss of function of E-cadherin and/or one or more of the associated catenins contributes to increased proliferation, invasion and metastasis in a wide variety of solid tumours. 1 Supporting observations include an inverse correlation between E-cadherin expression and increased invasiveness in vitro, 2 as well as an association between loss of E-cadherin expression and dedifferentiation, advanced tumour grade, metastasis and shortened survival. 3,4 The integrity of the entire E-cadherin-catenin-actin network is indispensable for E-cadherin-mediated cell-cell adhesion. Posttranslational modification such as tyrosine phosphorylation is widely recognised as the prevalent mechanism in regulating cadherin/catenin expression and/or function. 5 The catenins (␤-catenin, ␥-catenin and p120 ctn ) are the major targets of protein tyrosine kinases, which are heavily tyrosine phosphorylated in Src-transformed cells 6 and in response to growth factors such as EGF, 7,8 TGF-␣, PDGF 9,10 and HGF. 11 Furthermore, ␤-catenin and ␥-catenin directly associate with at least two receptor tyrosine kinases: EGFR 7 and c-erbB-2. 12 There is mounting evidence that E-cadherin expression can be modulated, either positively or negatively, by growth factors and cytokines. However, the mechanism of regulation of expression remains largely speculative. For instance, TGF-␤ induces dedifferentiation of normal mammary epithel...

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“…Indeed, FGF-1 could also contribute in the community e ect through its potent angiogenic activity. However, factors stimulating neoangiogenesis of NBT-II carcinoma do not allow tumor to develop faster than with the control NBT-II cells and therefore could not account for the community e ect (Jouanneau et al, 1997). …”

Section: Direct Fgf-1/fgfr Signalization Is Not Involved In the Commumentioning

confidence: 99%

“…The results showed that angiogenesis is unlikely to be causal to the community e ect since FGF-2 producing NBT-II cells did not form tumors faster than the untransfected NBT-II cells whereas these tumors were highly vascularized (Jouanneau et al, 1997). In this work we have attempted to determine whether a paracrine or a juxtacrine e ect mediated by FGF-1 may be responsible for the community e ect.…”

Section: Introductionmentioning

confidence: 99%

The community effect in FGF-1 mediated tumor progression of a rat bladder carcinoma does not involve a direct paracrine signaling

1999

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A community e ect was found to occur between heterogeneous tumor cell populations leading to an overall increased tumorigenicity without a clonal dominance of the more tumorigenic clone. In the rat bladder carcinoma cell line NBT-II, this e ect appears mediated by the Fibroblast Growth Factor-1 (FGF-1) through either a direct or an indirect signaling pathway. Neovascularization induced by FGF-1 was found not to be responsible for the community e ect. The present study shows that the community e ect does not involve a direct FGF-1 signaling since tumor cells expressing a dominant-negative FGF receptor mutant were still responding to the highly tumorigenic FGF-1 expressing cells. Tumors arising from inoculates of the FGF-1 producing NBT-II cells mixed with non tumorigenic epithelial MDCK cells contain only the tumorigenic cells indicating that MDCK cells may exerce a helper e ect for the growth of the tumor not dependant on their own growth. Therefore the helper function of MDCK cells must be distinguished from a community e ect where the contribution of low tumorigenic cells not only provides an in vivo growth advantage to few highly tumorigenic cells but become themselves highly tumorigenic indicating that the community e ect may require cell-cell speci®c cooperativity independent from an helper e ect.

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FGF-2 and FGF-1 expressed in rat bladder carcinoma cells have similar angiogenic potential but different tumorigenic properties in vivo

Cited by 41 publications

References 22 publications

Nuclear 24 kD fibroblast growth factor (FGF)-2 confers metastatic properties on rat bladder carcinoma cells

Nuclear 24 kD fibroblast growth factor (FGF)-2 confers metastatic properties on rat bladder carcinoma cells

FGF-1 and FGF-2 regulate the expression of E-cadherin and catenins in pancreatic adenocarcinoma

The community effect in FGF-1 mediated tumor progression of a rat bladder carcinoma does not involve a direct paracrine signaling

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