Papo N, Shai Y
Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot 76100, Israel.
Cell Mol Life Sci. 2005 Apr;62(7-8):784-90. doi: 10.1007/s00018-005-4560-2.
In the last decade intensive research has been conducted to determine the role of innate immunity host defense peptides (also termed antimicrobial peptides) in the killing of prokaryotic and eukaryotic cells. Many antimicrobial peptides damage the cellular membrane as part of their killing mechanism. However, it is not clear what makes cancer cells more susceptible to some of these peptides, and what the molecular mechanisms underlying these activities are. Two general mechanisms were suggested: (i) plasma membrane disruption via micellization or pore formation, and (ii) induction of apoptosis via mitochondrial membrane disruption. To be clinically used, these peptides need to combine high and specific anticancer activity with stability in serum. Although so far very limited, new studies have paved the way for promising anticancer host defense peptides with a new mode of action and with a broad spectrum of anticancer activity.
在过去十年中，人们进行了深入研究，以确定固有免疫宿主防御肽（也称为抗菌肽）在杀死原核细胞和真核细胞中的作用。许多抗菌肽会破坏细胞膜，这是它们杀伤机制的一部分。然而，目前尚不清楚是什么使得癌细胞对其中一些肽更敏感，以及这些活性背后的分子机制是什么。有人提出了两种一般机制：（i）通过胶束化或孔形成破坏质膜，以及（ii）通过破坏线粒体膜诱导细胞凋亡。为了临床应用，这些肽需要将高特异性抗癌活性与血清稳定性相结合。尽管到目前为止非常有限，但新的研究为具有新作用模式和广泛抗癌活性的有前景的抗癌宿主防御肽铺平了道路。
