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Hesperidin inhibits ovarian cancer cell viability through endoplasmic reticulum stress signaling pathways
Jun Zhao1, Yali Li1, Jinfang Gao2
1Department for Gynaecology and Obstetrics, General Hospital of People's Liberation Army, Beijing 100053, P.R. China.
Abstract:
Hesperidin is a vitamin P flavonoid compound primarily present in citrus fruits. The aim of the present study was to investigate whether hesperidin inhibits ovarian cancer cell viability via endoplasmic reticulum stress signaling pathways. A2780 cells were treated with various doses of hesperidin for 6, 12 or 24 h, and the viability of A2780 cells was assessed using the MTT assay. Hesperidin decreased the viability of A2780 cells and increased cytotoxicity in a dose- and time-dependent manner. In addition, hesperidin induced apoptosis and increased cleaved caspase-3 protein expression levels in A2780 cells. Furthermore, hesperidin markedly increased the protein expression of anti-growth arrest- and DNA damage-inducible gene 153, anti-CCAAT'enhancer-binding protein homologous protein, glucose-regulated protein 78 and cytochrome c in A2780 cells. The results of the present study indicated that hesperidin inhibits cell viability and induces apoptosis in ovarian cancer cells via endoplasmic reticulum stress signaling pathways. Thus, hesperidin may offer a novel therapeutic tool for ovarian carcinoma.
Insights
Hesperidin, a citrus flavonoid, inhibits ovarian cancer cell viability and induces apoptosis. It activates endoplasmic reticulum stress pathways, suggesting potential as a novel ovarian carcinoma therapeutic.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Hesperidin is a flavonoid found in citrus fruits, known for its potential health benefits.
- Ovarian cancer remains a significant health challenge, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the effect of hesperidin on ovarian cancer cell viability.
- To explore the role of endoplasmic reticulum (ER) stress signaling pathways in hesperidin's anti-cancer activity.
Main Methods:
- A2780 ovarian cancer cells were treated with varying doses of hesperidin over 6, 12, and 24 hours.
- Cell viability was assessed using the MTT assay.
- Apoptosis and ER stress markers (e.g., cleaved caspase-3, GADD153, CHOP, GRP78, cytochrome c) were analyzed via protein expression.
Main Results:
- Hesperidin significantly reduced ovarian cancer cell viability and increased cytotoxicity in a dose- and time-dependent manner.
- Hesperidin treatment induced apoptosis, evidenced by increased cleaved caspase-3 levels.
- Hesperidin upregulated key ER stress markers, including GADD153, CHOP, GRP78, and cytochrome c.
Conclusions:
- Hesperidin effectively inhibits ovarian cancer cell viability and promotes apoptosis.
- These effects are mediated through the activation of endoplasmic reticulum stress signaling pathways.
- Hesperidin shows promise as a potential therapeutic agent for ovarian carcinoma.
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