Abstract
A community effect 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 effect 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 effect. The present study shows that the community effect 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 effect 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 effect 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 effect may require cell-cell specific co-operativity independent from an helper effect.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 50 print issues and online access
$259.00 per year
only $5.18 per issue
Buy this article
- Purchase on SpringerLink
- Instant access to the full article PDF.
USD 39.95
Prices may be subject to local taxes which are calculated during checkout






Similar content being viewed by others
References
Aabo K, Vindelov U and Spang-Thomsen M. . 1995 Eur. J. Cancer 31: 222–229.
Amaya E, Musci TJ and Kirchner MW. . 1991 Cell 66: 257–270.
Bellot F, Crumley G, Kaplow JM, Schlessinger J, Jaye M and Dionne C. . 1991 EMBO J. 10: 2849–2854.
Bellusci S, Moens G, Gaudino G, Comoglio P, Nakamura T, Thiery JP and Jouanneau J. . 1994 Oncogene 9: 1091–1099.
Boyer B, Tucker GC, Vallès AM, Franke WW and Thiery JP. . 1989 J. Cell. Biol. 109: 1495–1509.
Camps JL, Chang SM, Hsu TC, Freeman MR, Hong SJ, Zhau HE, von Eschenbach AC and Chung LW. . 1990 Proc. Natl. Acad. Sci. USA 87: 75–79.
Colbere-Garapin F, Horodniceau F, Kourilsky P and Garapin AC. . 1981 J. Mol. Biol. 105: 1–4.
De Both NJ, Verney M, Groen N, Dinjens WN and Bosman FT. . 1997 Int. J. Cancer 72: 1137–1141.
Dionne CA, Crumley G, Bellot F, Kaplow JM, Searfoss G, Ruta M, Burgess WH, Jaye M and Schlessinger J. . 1990 EMBO J. 9: 2685–2692.
Folkman J and Klagsbrun M. . 1987 Science 235: 442–447.
Fridman R, Sweeney TM, Zain M, Martin GR and Kleinman HK. . 1992 Int. J. Cancer 51: 740–744.
Graham FL and Van der Eb AJ. . 1973 Virology 52: 456–467.
Gartner MF, Wilson EL and Dowdle EB. . 1992 Int. J. Cancer 51: 788–791.
Gurdon J, Lemaire P and Kato K. . 1993 Cell 75: 831–834.
Gregoire M and Lieubeau B. . 1995 Cancer Metastasis Rev. 14: 339–350.
Hennigan TW and Allen-Mersh TG. . 1994 Surg Oncol. 3: 275–277.
Jouanneau J, Gavrilovic J, Caruelle D, Jaye M, Moens G, Caruelle JP and Thiery JP. . 1991 Proc. Natl. Acad. Sci. USA 88: 2893–2897.
Jouanneau J, Moens G, Bourgeois Y, Poupon MF and Thiery . 1994 Proc. Natl. Acad. Sci. USA 91: 286–290.
Jouanneau J, Plouet J, Moens G and Thiery JP. . 1997 Oncogene 14: 671–676.
Li Y, Basilico C and Mansukhani A. . 1994 Mol. Cell. Biol. 14: 7660–7669.
Loizidou MC, Carpenter R, Laurie H, Cooper AJ, Alexander P and Taylor I. . 1996 Br. J. Surg. 83: 24–28.
Mehta RR, Graves JM, Hart GD, Shilkaitis A and Das Gupta TK. . 1993 Breast Cancer Res. Treat. 25: 65–71.
Nakajima M. . 1993 Hum. Cell. 6: 7–14.
Paweletz N and Boxberger HJ. . 1994 Crit. Rev. Oncog. 5: 69–105.
Rak JW and Kerbel RS. . 1993 In Vitro Cell. Dev. Biol. Anim. 29: 742–748.
Savagner P, Valles AM, Jouanneau J, Yamada K and Thiery JP. . 1994 Molec. Biol. Cell 5: 851–862.
Schor SL. . 1995 EXS 74: 273–296.
Shi E, Kan M, Xu J, Wang F, Hou J and McKeehan WL. . 1993 Mol. Cell. Biol. 13: 3907–3918.
Toyoshima K, Ito N, Hiasa Y, Kamamoto Y and Makiura S. . 1971 J. Natl. Cancer Inst. 47: 979–985.
Ulrich A and Schlessinger J. . 1990 Cell 61: 203–212.
Valles AM, Boyer B, Badet J, Tucker GC, Barritault D and Thiery JP. . 1990 Proc. Natl. Acad. Sci. USA 87: 1124–1128.
Werner S, Weinberg W, Liao X, Peters KG, Blessing M, Yuspa SH, Weiner RL and Williams LT. . 1993 EMBO J. 12: 2635–2643.
Wilson PA and Melton DA. . 1994 Curr. Biol. 4: 676–686.
Acknowledgements
We want to thank R Warn for his kind gift of MDCK cells, M Jaye for the pFlg plasmid and recombinant FGF-1, T. Nakamura for the HGF/SF, H Prats for the recombinant FGF-2, A Garapin for the pAG60 plasmid, Y Bourgeois for the nude mouse injections and D Morineau for his help with the photographs. This work was supported by the Centre National de la Recherche Scientifique (CNRS) and the Institut Curie and by grants from the Association pour la Recherche sur le cancer (ARC- 4045), the Ligue Nationale française contre le Cancer and the Groupement des Entreprises Françaises dans la Lutte contre le Cancer (Gefluc).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Jouanneau, J., Moens, G. & Thiery, J. The community effect in FGF-1 mediated tumor progression of a rat bladder carcinoma does not involve a direct paracrine signaling. Oncogene 18, 327–333 (1999). https://doi.org/10.1038/sj.onc.1202285
Received:
Revised:
Accepted:
Published:
Issue date:
DOI: https://doi.org/10.1038/sj.onc.1202285
Keywords
This article is cited by
-
The ORF 113 of Helicoverpa armigera single nucleopolyhedrovirus encodes a functional fibroblast growth factor
Virologica Sinica (2008)
-
Direct FGF receptor 1 activation through an anti-idiotypic strategy mimicks the biological activity of FGF-2 and inhibits the progression of the bladder carcinoma derived from NBT-II cells
Oncogene (2004)
-
Epithelial–mesenchymal transitions in tumour progression
Nature Reviews Cancer (2002)
-
Rapid tumor development and potent vascularization are independent events in carcinoma producing FGF-1 or FGF-2
Oncogene (2002)


