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Published on: March 27, 2020
The role of DAPK2 as a key regulatory element in various human cancers: a systematic review
Mohammadreza Saberiyan1, Mahboobeh Zarei2, Amir Safi3
1Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
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.
Insights
Death-associated kinase 2 (DAPK2) functions as a tumor suppressor by initiating apoptosis and autophagy. Its interactions suggest DAPK2 is a potential therapeutic target for cancers like gastric, ovarian, and breast cancer.
Area of Science:
- Molecular Biology
- Cellular Biology
- Oncology
Background:
- Cancer involves uncontrolled cell growth, influenced by molecular factors like the death-associated kinase (DAPK) family.
- DAPK2, a member of the DAPK family, plays crucial roles in cellular processes and acts as a tumor suppressor.
Purpose of the Study:
- To review the role of DAPK2 in cancer, focusing on its mechanisms in apoptosis and autophagy.
- To evaluate DAPK2 as a potential therapeutic target in various human cancers.
Main Methods:
- Literature review of studies from Scopus, PubMed, and Web of Science.
- Analysis of DAPK2's interactions with key proteins and signaling pathways.
Main Results:
- DAPK2 activates autophagy through interactions with AMPK, mTORC1, and p73.
- DAPK2 induces apoptosis via interactions with the p73 family and JNK.
- DAPK2 expression leads to cellular structural changes and apoptosis.
Conclusions:
- DAPK2 is vital in cell physiology, regulating apoptosis and autophagy.
- DAPK2's multifaceted role makes it a promising therapeutic target for gastric, ovarian, breast, and other cancers.
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