Suppression of HMGA2 Protein Synthesis Could Be a Tool for the Therapy of Well Differentiated Liposarcomas Overexpressing HMGA2

Francesca Pentimalli, Monica Dentice, Monica Fedele, Giovanna Maria Pierantoni, Letizia Cito, Pierlorenzo Pallante, Massimo Santoro, Giuseppe Viglietto, Paola Dal Cin, Alfredo Fusco

Research output: Contribution to journalArticlepeer-review

Abstract

Atypical lipomatous tumors (ALTs)/well-differentiated liposarcomas represent a distinctive subset of mesenchymal neoplasms featuring mature adipocytic proliferation. These tumors are characterized cytogenetically by the presence of supernumerary ring and/or long marker chromosomes that contain several copies of the chromosomal region 12q13-15, in which the HMGA2 gene is located. Deregulation of the HMGA2 gene is a common molecular alteration implicated in the development of a variety of benign tumors, such as lipomas, uterine leiomyomas, and pulmonary chondroid hamartomas. In this study, we observed HMGA2 overexpression in 7 of 12 ALT primary cell cultures examined. Subsequently, we generated an adenovirus containing the HMGA2 gene in the antisense orientation (Ad-A2as) to study the effect of HMGA2 protein suppression in ALT cells. The infection of six ALT cells, three of which were positive for HMGA2 expression, resulted in growth inhibition coupled with a significant increase in apoptosis. In addition, the growth of the ALT cells negative for HMGA2 expression was not affected by the infection with either the Ad-A2as or the control virus. On the basis of these findings, the targeting of the HMGA2 protein expression may represent a promising approach for treating the well-differentiated liposarcomas resistant to conventional therapies.

Original languageEnglish
Pages (from-to)7423-7427
Number of pages5
JournalCancer Research
Volume63
Issue number21
Publication statusPublished - Nov 1 2003

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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