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Apigenin sensitizes BEL-7402/ADM cells to doxorubicin through inhibiting miR-101/Nrf2 pathway
Ai-Mei Gao1,2, Xiao-Yu Zhang3, Zun-Ping Ke4
1Department of Pharmacy, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Abstract:
Chemo-resistance is one of the main obstacle in hepatocellular carcinoma therapy. Apigenin as a natural bioflavonoid has been exhibited anti-cancer properties in various malignant cancers. The aim of this study is to evaluate the potential chemo-sensitization effect of apigenin in doxorubicin-resistant hepatocellular carcinoma cell line BEL-7402/ADM and to investigate its possible mechanism. We found that apigenin significantly reversed doxorubicin sensitivity and induced caspase-dependent apoptosis in BEL-7402/ADM cells. Furthermore, apigenin induced miR-101 expression, and overexpression of miR-101 mimicked the doxorubicin-sensitizing effect of apigenin. Importantly, we showed that miR-101 was able to target the 3'-UTR of Nrf2. The results suggested that apigenin sensitizes BEL-7402/ADM cells to doxorubicin through miR-101/Nrf2 pathway, which furtherly supports apigenin as a potential chemo-sensitizer for hepatocellular carcinoma.
Insights
Apigenin, a natural compound, can overcome doxorubicin resistance in liver cancer cells by increasing apoptosis. It works by boosting miR-101 levels, which targets Nrf2, making chemotherapy more effective.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Chemo-resistance is a major challenge in hepatocellular carcinoma (HCC) treatment.
- Apigenin, a natural bioflavonoid, shows promise as an anti-cancer agent.
- Doxorubicin resistance in HCC limits therapeutic efficacy.
Purpose of the Study:
- To assess apigenin's potential to sensitize doxorubicin-resistant HCC cells (BEL-7402/ADM).
- To elucidate the underlying molecular mechanisms of apigenin's chemo-sensitizing effect.
Main Methods:
- Investigated apigenin's effect on doxorubicin sensitivity in BEL-7402/ADM cells.
- Assessed apigenin's role in inducing apoptosis via caspase pathways.
- Examined apigenin's impact on miR-101 expression and its interaction with Nrf2.
Main Results:
- Apigenin significantly reversed doxorubicin resistance in BEL-7402/ADM cells.
- Apigenin induced caspase-dependent apoptosis in resistant HCC cells.
- Apigenin upregulated miR-101 expression, which mimicked its sensitizing effect and targeted Nrf2.
Conclusions:
- Apigenin acts as a chemo-sensitizer, enhancing doxorubicin efficacy in resistant HCC.
- The miR-101/Nrf2 pathway is a key mechanism for apigenin's chemo-sensitizing action.
- Apigenin holds potential as a therapeutic agent to overcome chemo-resistance in HCC.
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