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. 2017 Nov;14(5):5569-5574.
doi: 10.3892/ol.2017.6873. Epub 2017 Sep 1.

Hesperidin Inhibits Ovarian Cancer Cell Viability Through Endoplasmic Reticulum Stress Signaling Pathways

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Free PMC article

Hesperidin Inhibits Ovarian Cancer Cell Viability Through Endoplasmic Reticulum Stress Signaling Pathways

Jun Zhao et al. Oncol Lett. .
Free PMC article

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.

Keywords: endoplasmic reticulum stress; hesperidin; ovarian cancer.

Figures

Figure 1.
Figure 1.
Molecular structure of hesperidin.
Figure 2.
Figure 2.
Hesperidin inhibits ovarian cancer cell proliferation. **P<0.01 vs. the control (0 µM hesperidin).
Figure 3.
Figure 3.
Hesperidin exhibits cytotoxicity towards ovarian cancer cells. **P<0.01 vs. the control (0 µM hesperidin).
Figure 4.
Figure 4.
Hesperidin induces ovarian cancer cell apoptosis. **P<0.01 vs. the control (0 µM hesperidin).
Figure 5.
Figure 5.
Hesperidin induces cleaved caspase-3 protein expression in ovarian cancer cells. (A) Western blot analysis of cleaved caspase-3 protein expression. (B) Quantification of cleaved caspase-3 protein expression in ovarian cancer cells relative to the control. **P<0.01 vs. the control (0 µM hesperidin).
Figure 6.
Figure 6.
Hesperidin induces GRP78 protein expression in ovarian cancer cells. (A) Western blot analysis of GRP78 protein expression levels. (B) Quantification of GRP78 protein expression in ovarian cancer cells vs. the control. **P<0.01 relative to the control (0 µM hesperidin). GRP78, glucose-regulated protein 78.
Figure 7.
Figure 7.
Hesperidin induces GADD153 protein expression in ovarian cancer cells. (A) Western blot analysis of GADD153 expression levels. (B) Quantification of GADD153 protein expression in ovarian cancer cells relative to the control. **P<0.01 vs. the control (0 µM hesperidin). GADD153, growth arrest- and DNA damage-inducible gene 153.
Figure 8.
Figure 8.
Hesperidin induces CHOP protein expression in ovarian cancer cells. (A) Western blot analysis of CHOP protein expression. (B) Quantification of CHOP protein expression in ovarian cancer cells relative to the control. **P<0.01 vs. the control (0 µM hesperidin). CHOP, CCAAT'enhancer-binding protein homologous protein.
Figure 9.
Figure 9.
Hesperidin induces cytochrome c protein expression in ovarian cancer cells. (A) Western blot analysis of cytochrome c protein expression. (B) Quantification of cytochrome c protein expression in ovarian cancer cells relative to the control. **P<0.01 vs. the control (0 µM hesperidin).

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