摘要
MET是约束肝细胞生长因子(HGF)的络氨酸激酶。它调控了许多生理过程,并参与了细胞增殖调控,不同细胞分化与运动。它在胚胎发育和成人生活中起重要作用。MET引起的调整通路的偏差是造成肿瘤发生的原因之一。最近MET信号在肿瘤发展中的新的重要作用被发现了,如癌干细胞的维持或者MET胞内定位的重要性。此外,MET被认为是造成横纹肌肉瘤(RMS,与成肌细胞有关的软组织肉瘤)发生发展的重要原因之一。它的起源仍有争议,但有人提议它源于卫星细胞或间充质干细胞分化的缺陷。在横纹肌肉瘤中,MET的下调引起肿瘤细胞分化,使RMS细胞转移可能性降低。因此,阻碍MET可能是未来在临床上有用的基于分化的RMS疗法。
关键词: MET受体,MET/HGF轴,癌症,横纹肌肉瘤,转移,肌生成
Current Drug Targets
Title:Targeting MET Receptor in Rhabdomyosarcoma: Rationale and Progress
Volume: 18 Issue: 1
Author(s): Barbara Szewczyk, Klaudia Skrzypek, Marcin Majka
Affiliation:
关键词: MET受体,MET/HGF轴,癌症,横纹肌肉瘤,转移,肌生成
摘要: 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.
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Barbara Szewczyk, Klaudia Skrzypek, Marcin Majka , Targeting MET Receptor in Rhabdomyosarcoma: Rationale and Progress, Current Drug Targets 2017; 18 (1) . https://dx.doi.org/10.2174/1389450117666151209124123
DOI https://dx.doi.org/10.2174/1389450117666151209124123 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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