Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Mol Biol Rep. 2024 Aug 6;51(1):886. doi: 10.1007/s11033-024-09761-6.
Cancer is considered the uncontrolled growth and spread of cells into neighboring tissues, a process governed at the molecular level by many different factors, including abnormalities in the protein family's death-associated kinase (DAPK). DAPK2 is a member of the DAPK protein family, which plays essential roles in several cellular processes. DAPK2 acts as a tumor suppressor, interacting with several proteins, such as TNF, IFN, etc. during apoptosis and autophagy. Expression of DAPK2 causes changes in the structure of the cell, ultimately leading to cell death by apoptosis. In this essay, studies are obtained from Scopus, PubMed, and the Web of Science. According to these investigations, DAPK2 activates autophagy by interacting with AMPK, mTORC1, and p73. Furthermore, DAPK2 induces apoptosis pathway via interacting with the p73 family and JNK. In general, due to the vital role of DAPK2 in cell physiology and its effect on various factors and signaling pathways, it can be a potent target in the treatment of various cancers, including gastric, ovarian, breast, and other prominent cancers.
癌症被认为是细胞不受控制的生长和扩散到邻近组织，这一过程在分子水平上受到许多不同因素的控制，包括蛋白家族死亡相关激酶（DAPK）的异常。DAPK2 是 DAPK 蛋白家族的成员，在几个细胞过程中发挥着重要作用。DAPK2 作为一种肿瘤抑制因子，在细胞凋亡和自噬过程中与 TNF、IFN 等多种蛋白质相互作用。DAPK2 的表达导致细胞结构发生变化，最终通过细胞凋亡导致细胞死亡。在这篇论文中，研究结果来自 Scopus、PubMed 和 Web of Science。根据这些研究，DAPK2 通过与 AMPK、mTORC1 和 p73 相互作用来激活自噬。此外，DAPK2 通过与 p73 家族和 JNK 相互作用诱导细胞凋亡途径。总的来说，由于 DAPK2 在细胞生理学中的重要作用及其对各种因素和信号通路的影响，它可能成为治疗各种癌症（包括胃癌、卵巢癌、乳腺癌和其他突出癌症）的有效靶点。
