MET is a tyrosine kinase receptor, which binds hepatocyte growth factor (HGF). It regulates
many physiological processes and participates in the regulation of proliferation, differentiation and motility
of various cells. It plays an important role in embryogenesis as well as in adult life. Aberrations
within the regulatory pathways activated by MET can be one of the causes of tumor development. Recently
novel important functions of MET signaling in tumor development have been described, such as
maintenance of cancer stem cells or importance of endosomal localization of MET. Moreover, MET is
considered as one of the important factors responsible for development of rhabdomyosarcoma (RMS), a
soft tissue sarcoma related to myogenic lineage. Its origin remains debatable but it is suggested that it
derives from defect in differentiation of the satellite cells or of the mesenchymal stem cells. In RMS
MET downregulation induces differentiation of tumor cells and in consequence, metastatic potential of
RMS cells is diminished. Therefore, blocking of MET may be clinically useful in novel differentiationbased
therapies of RMS in future.
Keywords: MET receptor, MET/HGF axis, cancer, rhabdomyosarcoma, metastasis, myogenesis.
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