The Role of Epidermal Growth Factor Receptor in Cancer and their Application for New Targeted Cancer Therapy
Correspondence Address :
Dr. Abbas Ali Imani Fooladi,
Applied Microbiology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences,
Tehran, Iran.
E-mail: imanifouladi.a@gmail.com
Epidermal Growth Factor Receptor (EGFR) has central role in cancer therapy because it causes tumour progression in many cases. The EGFR has seven ligands. Each factor that can block this binding, inhibits the intracellular signal transduction and prevents progression of the tumours. Immune system response is the most important factor for suppressing the initial stage of tumour growth and destroying some initial malignant cells, daily. On the other hand, tumours have different mechanisms to hide their antigens and escape from immune system responses. In contrary, tumours use some mechanisms to escape from immune system such as: 1) use of TGF-ß to initiate angiogenesis and immune suppression; 2) Induces Treg cell activation to modulate other immune cells; 3) secretion of the prostaglandin E2 to convert T cell into Treg. So, if a superantigen fused to one of the EGFR-ligands, causes the induction of immune system responses against the tumour cells. One of the new methods is based on the use of the fused super antigen with a ligand of the EGFR to inhibit ligand attaching to the EGFR and inducing immune system responses. To achieve this goal, we can block binding of EGFR to their ligands in the extracellular domain by fusing ligands with bacterial superantigens, toxins or cytokines of the viruses and plants that can induce immune system responses and kill malignant cells. So, the fused ligand can both block signal transduction and induce immune system response against malignant cells. In addition, with combining traditional drugs, high efficacy of the tumour treatment can be achieved. The aim of this review is to assess the mentioned strategy for targeting tumours.
Immune system responses, Ligand targeted therapy, Tyrosine kinase inhibitor
DOI: 10.7860/JCDR/2018/35499.11680
Date of Submission: Jan 08, 2018
Date of Peer Review: Mar 09, 2018
Date of Acceptance: Apr 13, 2018
Date of Publishing: Jun 01, 2018
FINANCIAL OR OTHER COMPETING INTERESTS: None.
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