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Silencing Bmi1 expression suppresses cancer stemness and enhances chemosensitivity in endometrial cancer cells
Miseon Kim1, Seul Lee2, Wook Ha Park2
1Department of Obstetrics and Gynecology, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Republic of Korea.
Background:
Bmi1, a polycomb group gene, is essential for self-renewal of stem cells and is frequently upregulated in various cancer cells. We aimed to investigate the effect of Bmi1 silencing on cancer stemness and chemosensitivity in endometrial cancer using targeted siRNA approach in HEC1A and Ishikawa cells.
Methods:
Cell viability after treatment with Bmi1 siRNA was assessed using the MTT assay, and cell apoptosis was visualized using the TdT-mediated dUTP nick-end labeling (TUNEL) method. Western blotting, migration assays and invasion assays were performed to detect changes in the stem-like properties of cancer cells. To evaluate the anticancer effect of Bmi1 silencing, HEC1A and Ishikawa cells were treated with 100 nM Bmi1 siRNA and/or 40 μM cisplatin.
Results:
In the MTT assay, compared to control, viability of HEC1A and Ishikawa cells significantly decreased after Bmi1 siRNA treatment in a dose-dependent manner. Bmi1 silencing using siRNA increased the expression of cleaved caspase-3 and cleaved poly adenosine diphosphate-ribose polymerase polymerase (PARP) as observed in the western blot analysis. Apoptosis significantly increased in the HEC1A and Ishikawa cells treated with 100 nM Bmi1 siRNA for 48 h than in the control cells in TUNEL assay. SOX2 and Oct4 expression decreased in the HEC1A and Ishikawa cells treated with Bmi1 siRNA, while E-cadherin expression increased. Further, migratory and invasive properties were significantly inhibited by Bmi1 siRNA treatment in both cell lines. Notably, viability of HEC1A and Ishikawa cells decreased more when they were concurrently treated with Bmi1 siRNA and cisplatin compared to when they were treated with Bmi1 siRNA or cisplatin alone.
Conclusion:
Bmi1 silencing suppresses cancer stemness in HEC1A and Ishikawa cells. Concurrent treatment with Bmi1 siRNA and cisplatin resulted in additive anticancer effect with a cell line-specific pattern, which was higher than that shown by cisplatin treatment alone.
Insights
Silencing Bmi1 (a gene crucial for stem cell renewal) in endometrial cancer cells reduced cancer stemness and increased apoptosis. Combining Bmi1 siRNA with cisplatin enhanced anticancer effects.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bmi1 is a polycomb group gene vital for stem cell self-renewal.
- Bmi1 is frequently overexpressed in various cancers, including endometrial cancer.
- Targeting Bmi1 may offer a therapeutic strategy for endometrial cancer.
Purpose of the Study:
- To investigate the impact of Bmi1 silencing on cancer stemness in endometrial cancer cells (HEC1A and Ishikawa).
- To assess the effect of Bmi1 silencing on chemosensitivity to cisplatin in endometrial cancer.
- To evaluate the potential of using siRNA to target Bmi1 in endometrial cancer therapy.
Main Methods:
- Bmi1 gene silencing was achieved using targeted small interfering RNA (siRNA).
- Cell viability was assessed via MTT assay; apoptosis was measured using TUNEL assay.
- Western blotting, migration, and invasion assays were employed to evaluate stemness markers and cellular behavior.
Main Results:
- Bmi1 siRNA significantly reduced HEC1A and Ishikawa cell viability in a dose-dependent manner.
- Bmi1 silencing increased apoptosis markers (cleaved caspase-3, cleaved PARP) and decreased stemness markers (SOX2, Oct4), while increasing E-cadherin.
- Combined Bmi1 siRNA and cisplatin treatment demonstrated an additive anticancer effect, surpassing cisplatin alone.
Conclusions:
- Bmi1 silencing effectively suppresses cancer stemness in endometrial cancer cell lines.
- Concurrent Bmi1 siRNA and cisplatin treatment enhances anticancer efficacy in a cell line-specific manner.
- Targeting Bmi1 alongside conventional chemotherapy presents a promising therapeutic approach for endometrial cancer.
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