Epithelial Cell Plasticity in Development and Tumor Progression View Full Text


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Article Info

DATE

1999-03

AUTHORS

Jean Paul Thiery, Dominique Chopin

ABSTRACT

Various mechanisms of epithelial cell plasticity in morphogenesis have been studied at the genetic and molecular levels. Several control genes have been identified including genes encoding transcription factors and growth factor receptors. These mechanisms may be reactivated during the progression of carcinomas. One of the mechanisms underlying epithelial plasticity is the epithelial–mesenchymal transition. This process has been extensively studied using the NBT-II bladder carcinoma cell line. Cells of this line undergo a reversible transition following exposure to several growth factors including FGF1, EGF, TGFα and SF/HGF, which activate tyrosine kinase surface receptors. Two separate transduction pathways have been identified. The transient activation of c-Src is involved in cytoskeleton remodeling whereas the Ras pathway controls the transcription of genes such as the transcription factor Slug which is involved in the internalization of desmosomes. These two pathways cooperate to induce the morphological transition, scattering and locomotion of fibroblast-like cells. Growth/scatter factor-producing NBT-II cells are more invasive than cells that do not contain this factor, in orthotopic confrontation assay. In vivo, these cells are very tumorigenic and may confer a more malignant phenotype on parental cells via a community effect. The role of several growth factors and their receptors has been investigated in human bladder carcinomas. A subset of these tumors with poor outcomes produce low levels of FGFR2-IIIb. The synthesis of this receptor de novo in bladder cell lines reduces proliferation in vitro and tumor growth in nude mice. FGFR2-IIIb functions as a tumor suppressor, consistent with the differentiation-inducing capacities of FGF receptors in the suprabasal cells of the skin. FGFR2-IIIb signaling may be involved in the maintenance of E-cadherin, the prototype epithelial adhesion molecule, which is only downregulated in a fraction of tumors with low FGFR2-IIIb synthesis. Human bladder tumors may also activate autocrine loops such as that for EGFR and their ligands, as already demonstrated for murine bladder tumors. Therefore, our results suggest that multifunctional growth factors and their receptors are involved in cell proliferation and epithelial cell plasticity, acting either as positive or negative regulators of tumor progression. The effect on the morphological transition is also clearly relevant to the mechanism governing dissemination and the formation of micrometastatic tumor cells. The extrapolation of these discoveries to human carcinomas should provide markers facilitating the more accurate prediction of the biological behavior of a given tumor and identify clinically and pathologically significant parameters. The identification of critical changes in the growth factor pathways involved in tumor progression will not only provide insight into the genetic and molecular basis of this process, but should also identify targets for new therapies. More... »

PAGES

31-42

References to SciGraph publications

  • 1998-12. Genetic instabilities in human cancers in NATURE
  • 1995-01. Prognostic value of epidermal growth factor-receptor, T138 and T43 expression in bladder cancer in BRITISH JOURNAL OF CANCER
  • 1998-01. FGFR1 is fused with a novel zinc-finger gene, ZNF198, in the t(8;13) leukaemia/lymphoma syndrome in NATURE GENETICS
  • 1997-05. Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomas in NATURE GENETICS
  • 1996-04. Skeletal overgrowth and deafness in mice lacking fibroblast growth factor receptor 3 in NATURE GENETICS
  • 1996-06. Graded activation of fibroblast growth factor receptor 3 by mutations causing achondroplasia and thanatophoric dysplasia in NATURE GENETICS
  • 1994. Modulations of the epithelial phenotype during embryogenesis and cancer progression in MAMMARY TUMORIGENESIS AND MALIGNANT PROGRESSION
  • 1998-02. High-dose chemotherapy and haematopoietic stem cell transplantation for inflammatory breast cancer: pathologic response and outcome in BONE MARROW TRANSPLANTATION
  • 1998-01. Induction of epithelial tubules by growth factor HGF depends on the STAT pathway in NATURE
  • 1999-12-08. Tumour suppressive properties of fibroblast growth factor receptor 2-IIIb in human bladder cancer in ONCOGENE
  • 1997-07. Frequent translocation t(4;14)(p16.3;q32.3) in multiple myeloma is associated with increased expression and activating mutations of fibroblast growth factor receptor 3 in NATURE GENETICS
  • 1997-02. FGF-2 and FGF-1 expressed in rat bladder carcinoma cells have similar angiogenic potential but different tumorigenic properties in vivo in ONCOGENE
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    http://scigraph.springernature.com/pub.10.1023/a:1006256219004

    DOI

    http://dx.doi.org/10.1023/a:1006256219004

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1042542823

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/10505544


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    170 transduction pathways
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