The role of DAPK2 as a key regulatory element in various human cancers: a systematic review.

ABSTRACT

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.