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[Cancer Research 64, 5154-5161, August 1, 2004]
© 2004 American Association for Cancer Research

Regular Articles

Truncated RON Tyrosine Kinase Drives Tumor Cell Progression and Abrogates Cell-Cell Adhesion Through E-Cadherin Transcriptional Repression

Chiara Bardella1, Barbara Costa1, Piera Maggiora1, Salvatore Patane’1, Martina Olivero1, Guglielmina N. Ranzani4, Michele De Bortoli2, Paolo M. Comoglio3 and Maria Flavia Di Renzo1

1 Laboratory of Cancer Genetics, 2 Functional Onco-Genomics Center, and 3 Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Turin, Italy, and 4 Department of Genetics and Microbiology, University of Pavia, Pavia, Italy

RON is a tyrosine kinase receptor that triggers scattering of normal cells and invasive growth of cancer cells on ligand binding. We identified a short RON mRNA, which is expressed in human lung, ovary, tissues of the gastrointestinal tract, and also in several human cancers, including ovarian carcinomas and cell lines from pancreatic carcinomas and leukemias. This transcript encodes a truncated protein (short-form RON; sf-RON), lacking most of the RON receptor extracellular domain but retaining the whole transmembrane and intracellular domains. Sf-RON shows strong intrinsic tyrosine kinase activity and is constitutively phosphorylated. Epithelial cells transduced with sf-RON display an aggressive phenotype; they shift to a nonepithelial morphology, are unable to form aggregates, grow faster in monolayer cultures, show anchorage-independent growth, and become motile. We show that in these cells, E-cadherin expression is lost through a dominant transcriptional repression pathway likely mediated by the transcriptional factor SLUG. Altogether, these data show that expression of a naturally occurring, constitutively active truncated RON kinase results in loss of epithelial phenotype and aggressive behavior and, thus, it might contribute to tumor progression.




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