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Hypermethylation of Ron proximal promoter associates with lack of full-length Ron and transcription of oncogenic short-Ron from an internal promoter

  1. Author:
    Angeloni, D.
    Danilkovitch-Miagkova, A.
    Ivanova, T.
    Braga, E.
    Zabarovsky, E.
    Lerman, M. I.

  2. Author Address

    NCI, Ctr Canc Res, Immunol Lab, Frederick, MD USA. Karolinska Inst, MTC, Stockholm, Sweden. Russian Acad Med Sci, Blokhin Canc Res Ctr, Inst Carcinogenesis, Moscow, Russia. CNR, Scuola Super St Anna, Inst Clin Physiol, Pisa, Italy. Russian State Genet Ctr, Lab Mol Diagnost, Moscow, Russia. Osiris Therapeut Inc, Baltimore, MD USA.;Angeloni, D, Scuola Super Sant Anna, Inst Clin Physiol, Via Mourzzi,1, I-56124 Pisa, Italy.;angeloni@ifc.cnr.it
    1. Year: 2007
    2. Date: Jul
  2. Journal: Oncogene
    1. 26
    2. 31
    3. Pages: 4499-4512
  4. Type of Article: Article
  5. ISSN: 0950-9232
  1. Abstract:

    The gene for tyrosine-kinase receptor Ron (MST1R) resides in the chromosome 3p21.3 region, frequently affected in common human malignancies. The gene generates two transcripts, 5 and 2 kb-long, full-length Ron (flRon) and short-form Ron (sfRon), respectively. Here, we show for the first time that the variegated Ron expression is associated with variations in the methylation patterns of two distinct CpG islands in Ron proximal promoter. Widespread hypermethylation associates with lack of flRon whereas hypermethylation of the distal island associates with transcription of sfRon, a constitutively active tyrosine-kinase that drives cell proliferation. sfRon inhibition with kinase-dead transgenes decreases cancer cell growth and induces cellular differentiation. sfRon could be a new drug target in cancer types in which it contributes to tumor progression.

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  2. DOI: 10.1038/sj.onc.1210238
  3. View record in Web of Science®
  4. WOS: 000247836100004

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