Insulin-like growth factor II and PAX3-FKHR cooperate in the oncogenesis of rhabdomyosarcoma

Weiguang Wang, Pat Kumar, Weizhi Wang, John Epstein, Lee Helman, Jim V. Moore, Shant Kumar

Research output: Contribution to journalArticlepeer-review

Abstract

The mouse myoblast C2C12 cell line transfected singly with cDNA for Pax- 3, PAX3-FKHR, or insulin-like growth factor (IGF) II or cotransfected with IGF-II plus Pax-3 or with IGF-II plus PAX3-FKHR genes showed an altered morphology, a lack of differentiation, and higher proliferation rates in vitro. On s.c. injection into nude mice, tumors grew from transfected cell lines but not from cells transfected with the empty vector. Tumors derived from IGF-II/PAX3-FKHR- and IGF-II-transfected cells grew most rapidly. Cotransfection of IGF-II plus Pax-3 induced tumors comprised highly differentiated striated muscle cells; Pax-3, PAX3-FKHR, or IGF-II transfection produced tumors at varying stages of differentiation. Tumors derived from IGF-II plus PAX3-FKHR-cotransfected cells were composed of undifferentiated cells. This was the only tumor type to infiltrate the underlying muscle. The most angiogenesis and the least apoptosis were observed in the latter tumors. These results support the hypothesis that PAX3-FKHR interacts with IGF-II to play a critical role in the oncogenesis of rhabdomyosarcoma.

Original languageEnglish (US)
Pages (from-to)4426-4433
Number of pages8
JournalCancer Research
Volume58
Issue number19
StatePublished - Oct 1 1998

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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