Therapeutic potential of hesperidin: Apoptosis induction in breast cancer cell lines

• Published in: Food and chemical toxicology Vol. 176; p. 113791
• Main Authors: Önder, Gözde Özge, Göktepe, Özge, Baran, Münevver, Bitgen, Nazmiye, Aydın, Funda, Yay, Arzu
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-06-2023
• Subjects: Apoptosis; bcl-2-Associated X Protein - genetics; bcl-2-Associated X Protein - metabolism; Breast Neoplasms - drug therapy; Breast Neoplasms - metabolism; Cell Line, Tumor; Cell Proliferation; Female; Hesperidin; Hesperidin - pharmacology; Hesperidin - therapeutic use; Humans; MCF-7; MCF-7 Cells; MDA-MB-231; Proto-Oncogene Proteins c-bcl-2 - genetics; Proto-Oncogene Proteins c-bcl-2 - metabolism; MCF-7; Hesperidin; MDA-MB-231; Apoptosis
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2023.113791

Hesperidin is a flavonoid commonly found in citrus fruits. Studies have shown that hesperidin has anti-inflammatory, analgesic, and antimicrobial properties, as well as its effectiveness in carcinogenesis. In this paper, we aim to investigate the molecular mechanisms of hesperidin-induced apoptosis in MCF-7 and MDA-MB-231 cancer cells.
The inhibitory effect of hesperidin on cellular proliferation was evaluated with the MTT assay. Cell cycle analysis of hesperidin-treated cells was then performed, as well as immunocytochemical analysis of the effect on the apoptosis pathway (TUNEL, Bax, and Bcl-2 expression).
Moreover, hesperidin induced cellular apoptosis in MCF-7 breast cancer cells by inhibiting Bcl-2 and enhancing Bax expression at protein levels. On the other hand, hesperidin caused apoptosis in the MDA-MB-231 breast cancer cell line, but it did not activate the Bax/Bcl-2 pathway. Hesperidin also induced cell cycle arrest at the S phase in the MCF-7 and MDA-MB-231 cell lines.
These findings showed that hesperidin is a potential therapeutic candidate for preventing the progression of breast cancer. In addition, hesperidin could significantly stimulate the death mechanisms in ER/PR (+) MCF-7 cells by changing the expression balance of Bax and Bcl-2 proteins, but lead ER/PR (−) MDA-MB-231 breast cancer cells to apoptosis in a different way.