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Human Gyrovirus-Apoptin Interferes with the Cell Cycle and Induces G2/M Arrest Prior to Apoptosis
Wiem Chaabane1, Saeid Ghavami2,3, Andrzej Małecki4
1Department of Biology, Faculty of Sciences, Tunis University, 2092, Tunis, Tunisia. wiemchaabane27@hotmail.fr.
Abstract:
The human gyrovirus-Apoptin (HGyv-Apoptin) is a protein that gained attention because it is selectively cytotoxic toward cancer cells. In this study, we have investigated the effect of HGyv-Apoptin on cell cycle progression of cancer cells. We also compared HGyv-Apoptin's action to its homologue chicken anemia virus Apoptin (CAV-Apoptin). We show that HGyv-Apoptin induces G2/M arrest in cancer cells. This is at least in part due to the fact that HGyv-Apoptin induces an abnormal spindle formation in mitotic cells that do not progress properly throughout the cell cycle. HGyv-Apoptin most likely inhibits APC function leading to a sustained cyclin-B1-expression. These results indicate that HGyv-Apoptin has a similar mechanism of action as its homolog CAV-Apoptin and further supports its cancer therapeutic potential.
Insights
Human gyrovirus-Apoptin (HGyv-Apoptin) selectively targets cancer cells, inducing cell cycle arrest. This protein shows potential as a cancer therapeutic by disrupting cell division similarly to chicken anemia virus Apoptin.
Area of Science:
- Molecular biology
- Virology
- Cancer research
Background:
- Human gyrovirus-Apoptin (HGyv-Apoptin) exhibits selective cytotoxicity towards cancer cells.
- Apoptin proteins are known for their anti-cancer properties.
Purpose of the Study:
- To investigate the effect of HGyv-Apoptin on cancer cell cycle progression.
- To compare HGyv-Apoptin's mechanism with chicken anemia virus Apoptin (CAV-Apoptin).
Main Methods:
- Cell cycle analysis of cancer cells treated with HGyv-Apoptin.
- Microscopic examination of mitotic spindle formation.
- Analysis of cyclin B1 expression.
Main Results:
- HGyv-Apoptin induces G2/M cell cycle arrest in cancer cells.
- Abnormal spindle formation and impaired mitotic progression were observed.
- HGyv-Apoptin likely inhibits APC function, leading to sustained cyclin B1 expression.
Conclusions:
- HGyv-Apoptin shares a similar mechanism of action with CAV-Apoptin.
- These findings support the potential of HGyv-Apoptin as a cancer therapeutic agent.
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