Truncated and chimeric HMGI-C genes induce neoplastic transformation of NIH3T3 murine fibroblasts

Monica Fedele, Maria Teresa Berlingieri, Stefania Scala, Lorenzo Chiariotti, Giuseppe Viglietto, Volkhard Rippel, Jorn Bullerdiek, Massimo Santoro, Alfredo Fusco

Research output: Contribution to journalArticlepeer-review


Overexpression of the high mobility group I (HMGI) proteins is often associated with the malignant phenotype. Moreover, many benign human tumors, mainly of mesenchymal origin, are characterized by rearrangements of the HMGI-C gene. In most cases, HMGI-C alterations involve breaks within the third intron of the gene resulting in aberrant transcripts carrying exons from 1-3, which encode the three DNA binding domains, fused to ectopic sequences. Here, we show that the expression of a truncated form of HMGI-C protein carrying only the three DNA-binding domains, or of a fusion protein carrying the three DNA-binding domains of HMGI-C and the LIM domains of the lipoma preferred partner gene (LPP) protein, causes malignant transformation of NIH3T3 cells. The unrearranged wild-type HMGI-C cDNA did not exert any transforming activity. These findings indicate that rearranged forms of HMGI-C play a role in cell transformation.

Original languageEnglish
Pages (from-to)413-418
Number of pages6
Issue number4
Publication statusPublished - Jul 30 1998


  • Chromatin
  • Lipoma
  • Oncogene
  • Tumor

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics


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