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Cremastranone-Derived Homoisoflavanes Suppress the Growth of Breast Cancer Cells via Cell Cycle Arrest and Caspase-Independent Cell Deathopen access

Authors
Choi, YeramPark, SangkyuLee, SeulShin, Ha-EunKwon, SangilChoi, Jun-KyuLee, Myeong-HeonSeo, Seung-YongLee, Younghee
Issue Date
Sep-2023
Publisher
한국응용약물학회
Keywords
Breast cancer; Cremastranone; Homoisoflavane; Cell cycle arrest; Caspase-independent cell death; Anti-cancer
Citation
Biomolecules & Therapeutics, v.31, no.5, pp.526 - 535
Journal Title
Biomolecules & Therapeutics
Volume
31
Number
5
Start Page
526
End Page
535
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89416
DOI
10.4062/biomolther.2023.057
ISSN
1976-9148
Abstract
Breast cancer is the most common cancer and a frequent cause of cancer-related deaths among women wordlwide. As therapeutic strategies for breast cancer have limitations, novel chemotherapeutic reagents and treatment strategies are needed. In this study, we investigated the anti-cancer effect of synthetic homoisoflavane derivatives of cremastranone on breast cancer cells. Homoisoflavane derivatives, SH-17059 and SH-19021, reduced cell proliferation through G2/M cell cycle arrest and induced caspase-independent cell death. These compounds increased heme oxygenase-1 (HO-1) and 5-aminolevulinic acid synthase 1 (ALAS1), suggesting downregulation of heme. They also induced reactive oxygen species (ROS) generation and lipid peroxidation. Furthermore, they reduced expression of glutathione peroxidase 4 (GPX4). Therefore, we suggest that the SH-17059 and SH-19021 induced the caspase-independent cell death through the accumulation of iron from heme degradation, and the ferroptosis might be one of the potential candidates for caspase-independent cell death.
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