Antisense epidermal growth factor receptor transfection impairs the proliferative ability of human rhabdomyosarcoma cells

Carla De Giovanni, Lorena Landuzzi, Flavia Frabetti, Giordano Nicoletti, Cristiana Griffoni, Ilaria Rossi, Maria Mazzotti, Luigi Scotto, Patrizia Nanni, Pier Luigi Lollini

Research output: Contribution to journalArticlepeer-review


Human rhabdomyosarcoma cells express membrane epidermal growth factor receptor (EGF-R), which could confer responsiveness to EGF and transforming growth factor-α (TGF-α) of autocrine or paracrine origin. To study the role played by this growth factor circuit in the proliferation and differentiation of myogenic neoplastic cells, human rhabdomyosarcoma EGF-R-expressing cells (RD/18 clone) have been transfected with a plasmid containing a fragment of the EGF-R cDNA in the antisense orientation. In vitro growth and differentiative ability were studied on six antisense-transfected clones (AS) in comparison to parental RD/18 cells and to cells transfected with the plasmid containing only the neomycin resistance gene (NEO). A reduced EGF-R membrane expression was found in AS clones by decreased immunofluorescence with an anti-EGF-R monoclonal antibody. All AS transfectants had a greatly impaired proliferative ability, even when cultured in fetal bovine serum- containing medium. Proliferation of AS clones was completely blocked in medium supplemented with 2% horse serum. The differentiation ability of AS clones was heterogeneous, ranging from clones with a percentage of myosin- positive cells higher than controls to clones with a negligible myosin expression. Therefore, the growth impairment determined by the loop interruption is not sufficient to switch on the differentiation program. The role played by EGF-R in the proliferation of human rhabdomyosarcoma cells suggests that this receptor could constitute a target for a therapeutic approach.

Original languageEnglish
Pages (from-to)3898-3901
Number of pages4
JournalCancer Research
Issue number17
Publication statusPublished - Sep 1 1996

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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