1. Academic Validation
  2. Diphenyl disulfide potentiates the apoptosis of breast cancer cells through Bax proteolytic activation with accompanying autophagy

Diphenyl disulfide potentiates the apoptosis of breast cancer cells through Bax proteolytic activation with accompanying autophagy

  • Environ Toxicol. 2023 Aug;38(8):2022-2030. doi: 10.1002/tox.23828.
Sheng-Yuan Chen 1 Chien-Chih Chiu 2 3 4 5 6 Chun-Tzu Hung 2 Wen-Hsiung Pan 3 Yen-Chun Chen 2 Yung-Ding Bow 7 Wan-Ju Li 2 Sheng-Kai Hsu 2 I-Ling Lin 8 9 Zhi-Hong Wen 10 Chang-Yi Wu 2 3
Affiliations

Affiliations

  • 1 Department of Medicine, Division of Cardiology, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.
  • 2 Department of Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan.
  • 3 Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.
  • 4 Center for Cancer Research, Kaohsiung Medical University, Kaohsiung, Taiwan.
  • 5 National Laboratory Animal Center, National Applied Research Laboratories, Taipei, Taiwan.
  • 6 Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
  • 7 Ph.D. Program in Life Sciences, College of Life Science, Kaohsiung Medical University, Kaohsiung, Taiwan.
  • 8 Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan.
  • 9 Department of Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
  • 10 Department of Marine Biotechnology and Research, National Sun Yat-sen University, Kaohsiung, Taiwan.
Abstract

Breast Cancer is a leading cause of cancer-related death worldwide, and chemoresistance often leads to poor patient outcomes. In this study, we investigated the Anticancer activity of synthetic diphenyl disulfide (DPDS) in breast Cancer cell lines. DPDS inhibited cellular proliferation and viability in a dose-dependent manner and reduced colony formation, an index of clonogenicity. Annexin-V and 7-AAD double staining showed that DPDS could induce the Apoptosis of breast Cancer cells. Western blotting of the expression of Bax p21 and its cleaved form p18 suggested the activation of p18 Bax-induced Apoptosis. Furthermore, the increased expression of the Autophagy marker LC3B-II indicated autophagic lysosome accumulation induced by DPDS. Our findings suggest that DPDS has potential as a candidate for treating breast Cancer, and further modifications and optimizations are warranted.

Keywords

apoptosis; autophagy; breast cancer; chemoresistance; diphenyl disulfide.

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