2. Academic Validation
  3. Desipramine induces apoptosis in hepatocellular carcinoma cells

Desipramine induces apoptosis in hepatocellular carcinoma cells

  • Oncol Rep. 2017 Aug;38(2):1029-1034. doi: 10.3892/or.2017.5723.
Dong Kwon Yang 1,  Shang-Jin Kim 1
Affiliations

Affiliation

  • 1 Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Biosafety Research Institute and Korea Zoonosis Research Institute, Chonbuk National University, Iksan, Jeollabuk-do 54596, Republic of Korea.
PMID: 28627696 DOI: 10.3892/or.2017.5723
Abstract

Antitumor effects of antidepressants have been reported in many Cancer cell lines. However, anti-proliferative effects of desipramine, a tricyclic antidepressant, in hepatocellular carcinoma are currently unknown. In this study, we examined the effects of desipramine in human hepatoma Hep3B cells. To evaluate anti-proliferative effects of desipramine in Hep3B cells, we determined cell viability, Reactive Oxygen Species (ROS) production, mitochondrial membrane potential (MMP), mitogen-activated protein kinase (MAPK) activity, and intracellular Ca2+ levels after desipramine treatment. Desipramine reduced cell viability, increased ROS production, and decreased MMP activity in Hep3B cells. In addition, desipramine activated MAPKs (ERK 1/2, JNK, and p38) and increased intracellular Ca2+ levels. Pro-apoptotic effects of desipramine were abolished after MAPK inhibitors (PD98059, SB203580, and SP600125) or N-acetyl-L-cysteine (NAC), as a ROS scavenger, treatments. These findings suggest that desipramine shows anti-proliferative effects in Hep3B cells mediated by promotion of Apoptosis, activation of MAPK signaling, and increase in intracellular Ca2+ levels.

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