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

Oncogene. 1998 Jul 30;17(4):413-8. doi: 10.1038/sj.onc.1201952.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Division
  • Cell Transformation, Neoplastic*
  • High Mobility Group Proteins / genetics*
  • Mice
  • Mutagenesis
  • Phenotype
  • Recombinant Fusion Proteins / genetics
  • Transfection


  • High Mobility Group Proteins
  • Recombinant Fusion Proteins