Format

Send to

Choose Destination
Oncol Lett. 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.

Author information

1
Department for Gynaecology and Obstetrics, General Hospital of People's Liberation Army, Beijing 100053, P.R. China.
2
Department for Gynaecology and Obstetrics, Navy General Hospital, Beijing 100048, 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.

KEYWORDS:

endoplasmic reticulum stress; hesperidin; ovarian cancer

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center