Defective myogenic differentiation of human rhabdomyosarcoma cells is characterized by sialidase Neu2 loss of expression

Authors

  • Elena Stoppani,

    1. Department of Biomedical Sciences and Biotechnology, Unit of Biochemistry, University of Brescia, viale Europa 11, 25123 Brescia, Italy
    Search for more papers by this author
  • Stefania Rossi,

    1. Department of Biomedical Sciences and Biotechnology, Unit of Biochemistry, University of Brescia, viale Europa 11, 25123 Brescia, Italy
    Search for more papers by this author
  • Sergio Marchesini,

    1. Department of Biomedical Sciences and Biotechnology, Unit of Biochemistry, University of Brescia, viale Europa 11, 25123 Brescia, Italy
    Search for more papers by this author
  • Augusto Preti,

    1. Department of Biomedical Sciences and Biotechnology, Unit of Biochemistry, University of Brescia, viale Europa 11, 25123 Brescia, Italy
    Search for more papers by this author
  • Alessandro Fanzani

    Corresponding author
    1. Department of Biomedical Sciences and Biotechnology, Unit of Biochemistry, University of Brescia, viale Europa 11, 25123 Brescia, Italy
    Search for more papers by this author

Tel.: +39 030 3717568; fax: +39 030 3701157. E-mail addresses: fanzani@med.unibs.it

Abstract

Sialidase Neu2 is a glycohydrolytic enzyme whose tissue distribution has been detected principally in differentiated skeletal muscle. In this study we show that Neu2 expression is absent in different embryonal and alveolar human tumor rhabdomyosarcoma (RMS) cells, which are genetically committed myoblasts characterized by delayed differentiation. Forced myogenic differentiation of an embryonal RMS cell line, as obtained via pharmacological and genetic p38 activation or via follistatin overexpression, was characterized by Neu2 loss of expression despite the significant rise of different muscle-specific markers, suggesting therefore that the defective myogenic program of RMS cells is accompanied by Neu2 suppression.

Ancillary