Peptides: A Supercilious Candidate for Activating Intrinsic Apoptosis by Targeting Mitochondrial Membrane Permeability for Cancer Therapy

被引:9
作者
Aslam, Muhammed [1 ]
Kanthlal, S. K. [1 ]
Panonummal, Rajitha [1 ]
机构
[1] Amrita Vishwa Vidyapeetham, Dept Pharmacol, Amrita Sch Pharm, Aims Hlth Sci Campus, Kochi 682041, Kerala, India
关键词
Apoptosis; Cytochrome c; Mitochondrial pores; Peptides; CELL-DEATH; BCL-2; BAK; INHIBITION; TRANSITION; PROTEINS; RELEASE;
D O I
10.1007/s10989-021-10297-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Escape from apoptosis is one of the main demeanor characters of cancer cells. Mitochondria is a key player in the initiation and regulation intrinsic apoptosis. Altering the outer mitochondrial membrane permeability can elicit cytochrome C release, which is a vital step in the intrinsic apoptosis pathway. Targeting the pore-forming protein and its regulators, known as Bcl2 family proteins, is a useful strategy to regulate apoptosis. This article provides a review of synthetic peptides that stimulate apoptosis via the mitochondrial pathways in the hopes of developing future cancer treatments. The role of mitochondria in apoptotic signaling is discussed as well as we outlined the mechanistic role of a few peptides that have been reported for cytotoxic effects, which may be useful to scientists working on therapeutic approaches. It was believed that if the extrinsic pathway failed to induce cell death, the intrinsic pathway. Apoptotic activity of peptides produced from the Bcl2 family, antimicrobial peptides, and other membrane protein-derived peptides has paved the way for the development of new generation anticancer therapeutic agents. However, if this fantastic scenario is to come true, molecular pharmacologists and peptide chemists will have to start working together rather than separately.
引用
收藏
页码:2883 / 2893
页数:11
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