Apoptosis and Pharmacological Therapies for Targeting Thereof for Cancer Therapeutics

Decis. Sci. Pub Date : 2022-04-06 DOI:10.3390/sci4020015
Vishakha Singh, Amit Khurana, Umashanker Navik, P. Allawadhi, K. Bharani, R. Weiskirchen
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引用次数: 24

Abstract

Apoptosis is an evolutionarily conserved sequential process of cell death to maintain a homeostatic balance between cell formation and cell death. It is a vital process for normal eukaryotic development as it contributes to the renewal of cells and tissues. Further, it plays a crucial role in the elimination of unnecessary cells through phagocytosis and prevents undesirable immune responses. Apoptosis is regulated by a complex signaling mechanism, which is driven by interactions among several protein families such as caspases, inhibitors of apoptosis proteins, B-cell lymphoma 2 (BCL-2) family proteins, and several other proteases such as perforins and granzyme. The signaling pathway consists of both pro-apoptotic and pro-survival members, which stabilize the selection of cellular survival or death. However, any aberration in this pathway can lead to abnormal cell proliferation, ultimately leading to the development of cancer, autoimmune disorders, etc. This review aims to elaborate on apoptotic signaling pathways and mechanisms, interacting members involved in signaling, and how apoptosis is associated with carcinogenesis, along with insights into targeting apoptosis for disease resolution.
细胞凋亡及其在癌症治疗中的靶向药物治疗
细胞凋亡是一个进化上保守的细胞死亡的顺序过程,以维持细胞形成和细胞死亡之间的稳态平衡。它是正常真核生物发育的重要过程,因为它有助于细胞和组织的更新。此外,它在通过吞噬消除不必要的细胞和防止不良免疫反应中起着至关重要的作用。细胞凋亡是由复杂的信号机制调控的,它是由几个蛋白家族(如半胱天蛋白酶、凋亡蛋白抑制剂、b细胞淋巴瘤2 (BCL-2)家族蛋白和其他一些蛋白酶(如穿孔素和颗粒酶)之间的相互作用驱动的。该信号通路由促凋亡和促存活成员组成,它们稳定细胞生存或死亡的选择。然而,该通路的任何异常都可能导致细胞增殖异常,最终导致癌症、自身免疫性疾病等的发展。本综述旨在阐述细胞凋亡信号通路和机制,参与信号传导的相互作用成员,细胞凋亡如何与癌变相关,以及靶向细胞凋亡治疗疾病的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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