Van Der Steen Nele, Pauwels Patrick, Gil-Bazo Ignacio, Castañon Eduardo, Raez Luis, Cappuzzo Federico, Rolfo Christian
Center for Oncological Research Antwerp, University of Antwerp, Universiteitsplein 1, Wilrijk 2610, Belgium.
Molecular Pathology Unit, Pathology Department, Antwerp University Hospital, Wilrijkstraat 10, Edegem 2650, Belgium.
Cancers (Basel). 2015 Mar 25;7(2):556-73. doi: 10.3390/cancers7020556.
In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also confers resistance against several currently used targeted therapies, e.g., epidermal growth factor receptor (EGFR) inhibitors. In this review, we will discuss the basic structure of cMET and the most important signaling pathways. We will also look into aberrations in the signaling and the effects thereof in cancer growth, with the focus on NSCLC. Finally, we will discuss the role of cMET as resistance mechanism.
在过去十年中，酪氨酸激酶受体cMET及其配体肝细胞生长因子（HGF）已成为非小细胞肺癌（NSCLC）的一个靶点。通过cMET的信号传导刺激了多种肿瘤学过程，其中包括细胞运动、侵袭和转移。它还赋予对几种目前使用的靶向疗法的抗性，例如表皮生长因子受体（EGFR）抑制剂。在本综述中，我们将讨论cMET的基本结构和最重要的信号通路。我们还将研究信号传导中的异常及其在癌症生长中的作用，重点是NSCLC。最后，我们将讨论cMET作为抗性机制的作用。
