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Targeting the BMI1-Noxa axis by Dioscin induces apoptosis in oral squamous cell carcinoma cells
Jinglin Fang1,2, Ruirui Wang3, Xiaoying Li3
1School of Stomatology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Abstract:
Dioscin is a natural plant-derived steroidal saponin that exerts antitumor effects in multiple cancers. It is widely involved in multiple apoptotic pathways and exerts its anti-tumor effects. In this study, we discovered that Dioscin treatment increased the expression of Noxa, thereby inducing the apoptosis of OSCC cells. Previous reports indicate that dysfunction of the BMI1-Noxa axis is frequently observed in multiple cancers. Our study revealed that Dioscin upregulates Noxa by impairing the protein expression of BMI1 in OSCC cells. Dioscin promotes the ubiquitination of BMI1 and facilitates its degradation, leading to upregulation of Noxa expression at the mRNA level and activation of apoptosis. Additionally, Dioscin exhibited potent tumor suppression in xenograft tumor models. In conclusion, our research provides new insights and strategies for inhibiting OSCC cells by investigating the ant-tumor mechanism of the natural compound Dioscin.
Insights
Dioscin, a natural compound, induces apoptosis in oral squamous cell carcinoma (OSCC) by targeting the BMI1-Noxa pathway. This study reveals Dioscin
Area of Science:
- Oncology
- Molecular Biology
- Natural Products Chemistry
Background:
- Dioscin is a steroidal saponin with known antitumor properties.
- The BMI1-Noxa axis is implicated in various cancers.
- Oral squamous cell carcinoma (OSCC) remains a significant health concern.
Purpose of the Study:
- To investigate the anti-tumor mechanism of Dioscin in OSCC.
- To elucidate the role of the BMI1-Noxa axis in Dioscin-induced apoptosis.
- To evaluate Dioscin's efficacy in preclinical OSCC models.
Main Methods:
- Cell culture of OSCC lines.
- Dioscin treatment and assessment of apoptosis markers.
- Western blot analysis to determine BMI1 and Noxa protein levels.
- Ubiquitination assays for BMI1.
- Quantitative real-time PCR for Noxa mRNA expression.
- In vivo xenograft tumor models.
Main Results:
- Dioscin treatment upregulated Noxa expression in OSCC cells.
- Dioscin impaired BMI1 protein expression by promoting its ubiquitination and degradation.
- Upregulation of Noxa by Dioscin led to apoptosis activation in OSCC cells.
- Dioscin demonstrated significant tumor suppression in xenograft models.
Conclusions:
- Dioscin effectively inhibits OSCC cell growth through the BMI1-Noxa pathway.
- Dioscin promotes BMI1 degradation, leading to Noxa upregulation and apoptosis.
- Dioscin represents a potential therapeutic strategy for OSCC treatment.
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