Effects of Tetrandrine on the Apoptosis of Cisplatin-resistant Oral Cancer Cells
Chin-Wen Chang1, Chun Chen2, Chih-Wei Chang3, Po-Yen Chiu3, Jai-Sing Yang4, Fu-An Chen3★★ Corresponding author
- 1Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, TAIWAN.
- 2School of Pharmacy, College of Pharmacy, Kaohsiung Medical University, Kaohsiung, TAIWAN.
- 3Department of Pharmacy and Master Program, Tajen University, Pingtung, TAIWAN.
- 4Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, TAIWAN.
CORRESPONDENCE
Fu-An Chen
Department of Pharmacy and Master Program, Tajen University, Pingtung 907, TAIWAN.
Received: 25-08-2022; Accepted: 08-11-2022.
Volume 19, Issue 2 · pp. 295–302 · PUBLISHED 2023 · DOI: 10.1177/09731296231158699
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ABSTRACT
Background: Cisplatin, the first-line drug for chemotherapy, often has limited treatment efficacy because of resistance and cancer recurrence mechanisms. Tetrandrine is a unique secondary metabolite of Stephania tetrandra. As a traditional Chinese medicine agent, tetrandrine has been reported to have antioxidant, anti-inflammatory, antitumor, and antiangiogenesis activities and has been shown to inhibit the proliferation and angiogenesis of colorectal, lung, and breast cancer cells; potential mechanisms underlying its activities include the promotion of tumor cell apoptosis, promotion of cell cycle arrest, and intensification of reactive oxygen species (ROS) production. Objectives: The main treatments for oral cancer are chemotherapy, surgery, and radiotherapy; these treatments are often used in combination. Cancer cells easily develop cisplatin resistance; therefore, we investigated tetrandrine’s potential as a therapy for overcoming resistance to oral cancer drugs. Materials and Methods: We used the cisplatin-resistant oral cancer CAR cell line (CAL27) as a research objected and applied inhibitor treatment to clarify the role of tetrandrine in cell death and mitochondrial dysfunction. Results: Tetrandrine could effectively inhibit CAR cell proliferation and induce apoptosis, with a corresponding increase in ROS production in mitochondria. Moreover, tetrandrine increased caspase-9 and caspase-3 activity in CAR cells and induced apoptotic mRNA, caspase-3/-9, AIF, and Endo G overexpression. Our results indicate that tetrandrine induces apoptosis in CAR cells through a mitochondrial-dependent signaling pathway.
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Chang, C., Chen, C., Chang, C., Chiu, P., Yang, J., & Chen, F. (2023). Effects of Tetrandrine on the Apoptosis of Cisplatin-resistant Oral Cancer Cells. Pharmacognosy Magazine, 19(2), 295–302. https://doi.org/10.1177/09731296231158699