Publication: Mechanism of Anti-Cancer in Breast Cancer Cells With HER2 Overexpression by Dietary Supplement of Five Edible Plants
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Issued Date
2025-07-01
Resource Type
eISSN
20487177
Scopus ID
2-s2.0-105010698725
Journal Title
Food Science and Nutrition
Volume
13
Issue
7
Rights Holder(s)
SCOPUS
Bibliographic Citation
Food Science and Nutrition Vol.13 No.7 (2025)
Suggested Citation
Sitthisuk P., Kwankaew N., Innajak S., Nilchad K., Poorahong W., Kongdang P., Watanapokasin R. Mechanism of Anti-Cancer in Breast Cancer Cells With HER2 Overexpression by Dietary Supplement of Five Edible Plants. Food Science and Nutrition Vol.13 No.7 (2025). doi:10.1002/fsn3.70617 Retrieved from: https://hdl.handle.net/20.500.14740/21200
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Abstract
Edible plants are known to have many pharmacological properties, including anti-cancer. Mylife/Mylife100, a Thai dietary supplement composed of five types of edible plants (Sesamum indicum L., Psidium guajava L., Centella asiatica (L.) Urb., Glycine max (L.) Merr., and Garcinia mangostana L.) was evaluated for its anti-cancer effect on breast cancer cells with HER2 overexpression (SK-BR-3 cell line). The results demonstrated that the supplement showed cytotoxic activity against SK-BR-3 cell growth in a dose-dependent manner, with an IC<inf>50</inf> value of 116.5 ± 2.30 μg/mL. The effect of the supplement on apoptosis induction in SK-BR-3 cells was investigated. The findings revealed that the supplement induced nuclear condensation and loss of mitochondrial membrane potential, both hallmarks of apoptosis. Additionally, the supplement increased the sub-G1 population analyzed by flow cytometry and was further validated by attenuation of anti-apoptotic proteins (Bcl-xL and Mcl-1) and the induction of pro-apoptotic proteins (Bax, cleavage caspase 7 and cleavage PARP). Moreover, the supplement also inhibited the PI3K/Akt pathway and enhanced MAPK signaling pathways. These findings indicated that the Mylife/Mylife100 supplement suppresses cell growth and induces apoptosis via activation of the intrinsic pathway and regulation of the PI3K/Akt and MAPK signaling pathways against SK-BR-3 cells.