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Overexpressed exocyst complex component 3-like 1 spontaneously induces apoptosis
Shunichi Matsumoto1, Junichi Okada2, Eijiro Yamada1
1Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine.
Biomedical Research (Tokyo, Japan)
|June 7, 2021
Summary
Exocyst complex component 3-like 1 (EXOC3L1) regulates insulin secretion and is found throughout the body. Overexpressed EXOC3L1 induces apoptosis, unlike its isoform Sec6.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Exocyst complex component 3-like 1 (EXOC3L1) is involved in insulin secretion and widely distributed in various human tissues.
- EXOC3L1 shares sequence similarity with Sec6, a known apoptosis suppressor.
- Sec6 suppresses apoptosis through HSP27 phosphorylation.
Purpose of the Study:
- To investigate the role of EXOC3L1 expression in apoptosis.
- To compare the apoptotic effects of EXOC3L1 with its isoform, Sec6.
Main Methods:
- Overexpression of EXOC3L1 in Chinese hamster ovary (CHO) cells.
- Assessment of cell viability and apoptosis markers, including DNA laddering and caspase 3 activity.
Main Results:
- Overexpressed EXOC3L1 significantly reduced CHO cell numbers.
- EXOC3L1 overexpression led to increased DNA fragmentation, caspase 3 activity, and caspase 3 cleavage.
- These apoptotic effects occurred spontaneously without external apoptotic inducers.
Conclusions:
- EXOC3L1, unlike Sec6, can independently induce apoptosis when overexpressed.
- EXOC3L1's role in apoptosis warrants further investigation, particularly in relation to its function in insulin secretion.
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