IGF1R and c-met as therapeutic targets for colorectal cancer

被引:34
|
作者
Shali, Hajar [1 ,2 ]
Ahmadi, Majid [3 ,4 ]
Kafil, Hossein Samadi [5 ]
Dorosti, Abbasali [6 ]
Yousefi, Mehdi [3 ,4 ]
机构
[1] Tabriz Univ Med Sci, Liver & Gastrointestinal Dis Res Ctr, Tabriz, Iran
[2] Tabriz Univ Med Sci, Students Res Comm, Tabriz, Iran
[3] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran
[4] Tabriz Univ Med Sci, Sch Med, Dept Immunol, Tabriz, Iran
[5] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran
[6] Tabriz Univ Med Sci, Imam Reza Hosp, Sch Med, Dept Anesthesiol, Tabriz, Iran
关键词
Colorectal cancer; IGF1R; c-Met; Receptor tyrosine kinase; GROWTH-FACTOR-I; MONOCLONAL-ANTIBODY FIGITUMUMAB; FACTOR SIGNALING PATHWAY; FACTOR-BINDING-PROTEINS; INHIBITS TUMOR-GROWTH; FACTOR RECEPTOR; TYROSINE KINASE; COLON-CANCER; CARCINOMA CELLS; MEDIATED MIGRATION;
D O I
10.1016/j.biopha.2016.05.034
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The type 1 IGF receptor (IGF1R) and mesenchymal-epithelial transition (MET) are hetrodimeric and transmembrane receptor tyrosine kinases, which are frequently overexpressed by several tumor types, including colorectal cancer (CRC). These receptors bind to their specific ligands, insulin growth factors (IGFs) and hepatocyte growth factor (HGF), respectively, and promote signaling cascades which mediates many functions such as proliferation and protection against apoptosis, cell scattering, tumor cell motility, invasion and metastasis. In patients with metastatic colorectal cancer (mCRC), IGF1R and c-met expression confer resistance to cetuximab (monoclonal antibodies against EGFR). Therefore, the c-met and IGF1R are now an attractive novel target for anticancer therapy. In this review, we will describe correlation between two receptors and their activation effects in tumor cells, and finally introduce useful and available strategies for their targeting. (C) 2016 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:528 / 536
页数:9
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