Mitochondrial targeted peptides for cancer therapy

被引:63
|
作者
Farsinejad, Sadaf [1 ]
Gheisary, Zohre [1 ]
Samani, Sanaz Ebrahimi [1 ]
Alizadeh, Ali Mohammad [1 ]
机构
[1] Univ Tehran Med Sci, Canc Res Ctr, Tehran, Iran
关键词
Mitochondria; Peptide; Cancer; Review; PERMEABILITY TRANSITION PORE; BCL-2 FAMILY INHIBITOR; CELL-DEATH MECHANISMS; CYTOCHROME-C; ANTITUMOR-ACTIVITY; MUC1-C ONCOPROTEIN; MULTIPLE-MYELOMA; BREAST-CANCER; RAT-HEART; APOPTOSIS;
D O I
10.1007/s13277-015-3719-1
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Mitochondria are a key pharmacological target in all cancer cells, since the structure and function of this organelle is different between healthy and malignant cells. Oxidative damage, disruption of mitochondrial ATP synthesis, calcium dyshomeostasis, mtDNA damage, and induction of the mitochondrial outer membrane permeabilization (MOMP) lead to the mitochondrial dysfunctionality and increase the probability of the programmed cell death or apoptosis. A variety of the signaling pathways have been developed to promote cell death including overexpression of pro-apoptotic members of Bcl-2 family, overloaded calcium, and elevated reactive oxygen species (ROS) play a key role in the promoting mitochondrial cytochrome c release through MOMP and eventually leads to cell death. There are a wide range of the therapeutic-based peptide drugs, known mitochondrial targeted peptides (MTPs), which specifically target mitochondrial pathways into death. They have prominent advantages such as low toxicity, high specificity, and easy to synthesis. Some of these therapeutic peptides have shown to increased the clinical activity alone or in combination with other agents. In this review, we will outline the biological properties of MTPs for cancer therapy. Understanding the molecular mechanisms and signaling pathways controlling cell death by MTPs can be critical for the development of the therapeutic strategies for cancer patients that would be valuable for researchers in both fields of molecular and clinical oncology.
引用
收藏
页码:5715 / 5725
页数:11
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