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PM · Lens · Effects of Tetrandrine on the Apoptosis of Cisplatin-resistant Oral Cancer Cells

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Article · Volume 19, Issue 2 · pp. 295–302

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

  1. 1Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, TAIWAN.
  2. 2School of Pharmacy, College of Pharmacy, Kaohsiung Medical University, Kaohsiung, TAIWAN.
  3. 3Department of Pharmacy and Master Program, Tajen University, Pingtung, TAIWAN.
  4. 4Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, TAIWAN.

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.

Keywords: Apoptosis; Tetrandrine; CAR cells (CAL27 cisplatin-resistant human oral cancer cells)

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