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Published on: September 30, 2016
IGF1R and c-met as therapeutic targets for colorectal cancer
Hajar Shali1, Majid Ahmadi2, Hossein Samadi Kafil3
1Liver and Gastrointestinal Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Student's Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract:
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.
Insights
The insulin growth factor type 1 receptor (IGF1R) and mesenchymal-epithelial transition (MET) are key in colorectal cancer progression and cetuximab resistance. Targeting these receptors offers a novel anticancer therapy strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Type 1 IGF receptor (IGF1R) and MET are transmembrane receptor tyrosine kinases overexpressed in various cancers, including colorectal cancer (CRC).
- These receptors mediate critical cellular functions like proliferation, anti-apoptosis, motility, invasion, and metastasis via signaling cascades.
- Overexpression of IGF1R and c-met in metastatic CRC (mCRC) confers resistance to cetuximab, an EGFR-targeting monoclonal antibody.
Purpose of the Study:
- To review the correlation between IGF1R and c-met signaling pathways in tumor cells.
- To explore the activation effects of these receptors in cancer progression.
- To introduce therapeutic strategies for targeting IGF1R and c-met in cancer treatment.
Main Methods:
- Literature review focusing on receptor tyrosine kinases, specifically IGF1R and MET.
- Analysis of signaling pathways involved in cancer proliferation, invasion, and metastasis.
- Examination of therapeutic approaches targeting IGF1R and MET.
Main Results:
- IGF1R and MET signaling pathways are implicated in promoting tumor cell proliferation and survival.
- Co-expression of IGF1R and c-met contributes to resistance against EGFR-targeted therapies like cetuximab.
- These receptors represent attractive targets for novel anticancer drug development.
Conclusions:
- The interplay between IGF1R and MET signaling is crucial in colorectal cancer pathogenesis and therapeutic resistance.
- Targeting IGF1R and MET offers a promising strategy for overcoming resistance and improving treatment outcomes in mCRC.
- Further research into combined targeting strategies may enhance efficacy in cancer therapy.
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