Induction of ferroptosis and apoptosis in endometrial cancer cells by dihydroisotanshinone I

Ching-Yuan Wu; Yao-Hsu Yang; Yu-Shih Lin; Li-Hsin Shu; Hung-Te Liu; Yu-Huei Wu; Yu-Heng Wu

doi:10.1016/j.heliyon.2023.e21652

Induction of ferroptosis and apoptosis in endometrial cancer cells by dihydroisotanshinone I

Heliyon. 2023 Oct 31;9(11):e21652. doi: 10.1016/j.heliyon.2023.e21652. eCollection 2023 Nov.

Authors

Ching-Yuan Wu^{1

2

3}, Yao-Hsu Yang^{1

2}, Yu-Shih Lin⁴, Li-Hsin Shu¹, Hung-Te Liu¹, Yu-Huei Wu⁵, Yu-Heng Wu⁶

Affiliations

¹ Department of Chinese Medicine, Chiayi Chang Gung Memorial Hospital, Chiayi, Taiwan.
² School of Chinese Medicine, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan.
³ Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
⁴ Department of Pharmacy, Chiayi Chang Gung Memorial Hospital, Chiayi, Taiwan.
⁵ Department of Biomedical Sciences, Chang Gung University, Tao-Yuan, Taiwan.
⁶ Department of Electrical Engineering, National Sun Yat-Sen University, Kaohsiung, Taiwan.

Abstract

Danshen, also known as Salvia miltiorrhiza, is a medicinal herb used in traditional Chinese medicine. Its potential impact on endometrial cancer has not been thoroughly investigated. This study aimed to examine the effect of dihydroisotanshinone I (DT), a compound found in Danshen, on the viability of ARK1 and ARK2 endometrial cancer cells and its mechanisms. The results showed that 10 μM DT inhibited cell viability of ARK1 and ARK2 cells by inducing apoptosis and ferroptosis, which was achieved by blocking the expression of GPX4. In vivo experiments using a xenograft nude mouse model indicated that DT treatment significantly reduced tumor volume without causing any adverse effects. These findings suggest that DT may be a potential therapeutic agent for inhibiting endometrial cancer cell viability, but further research is needed to confirm these results.

Keywords: Dihydroisotanshinone I; Endometrial cancer; GPX4; apoptosis; ferroptosis.