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

Abstract

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.

• Authors: M Fedele, M T Berlingieri, S Scala, L Chiariotti, G Viglietto, V Rippel, J Bullerdiek, M Santoro, A Fusco
• Journal: Oncogene (Oncogene) Vol. 17 Issue 4 Pg. 413-8 (Jul 30 1998) ISSN: 0950-9232 [Print] England
• PMID: 9696033 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• High Mobility Group Proteins
• Recombinant Fusion Proteins

Topics

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