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Insight into the structure, function and the tumor suppression effect of gasdermin E
Yuge Long1, Xiaoyuan Jia2, Liang Chu3
1Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China; College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou 310018, Zhejiang, China.
Biochemical Pharmacology
|June 9, 2024
Summary
Gasdermin E (GSDME) induces cell death through pyroptosis and apoptosis, with potential tumor-suppressive effects. This review explores GSDME
Area of Science:
- Molecular Biology
- Cell Death Mechanisms
- Oncology
Background:
- Gasdermin E (GSDME), also known as DFNA5, was initially identified as a deafness-related gene.
- GSDME expression is low in tumor cells but significant in kidney, placenta, muscle, and brain.
- GSDME is a member of the gasdermin family, involved in apoptosis and pyroptosis.
Purpose of the Study:
- To review the structure and function of Gasdermin E (GSDME).
- To elucidate the mechanisms by which GSDME induces pyroptosis and apoptosis.
- To discuss the tumor-suppressive role and therapeutic potential of GSDME.
Main Methods:
- Literature review of studies on Gasdermin E (GSDME).
- Analysis of GSDME's role in apoptosis and pyroptosis pathways.
- Examination of GSDME's expression patterns and tumor-related functions.
Main Results:
- Caspase-3 and Granzyme B cleave GSDME to activate pyroptosis via membrane pore formation.
- GSDME induces intrinsic apoptosis by releasing factors like cytochrome c from mitochondria.
- GSDME exhibits tumor-suppressive effects, indicating therapeutic promise.
Conclusions:
- GSDME is a key mediator of pyroptosis and apoptosis.
- GSDME's function in cell death pathways highlights its potential as an anti-cancer target.
- Further research into GSDME could unlock novel cancer therapies.
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