In vitro inhibition of growth and induction of apoptosis in cancer cell lines by thymoquinone

Int J Oncol. 2003 Jan;22(1):107-13.


Thymoquinone (TQ) is likely responsible for the chemotherapeutic effects of N. sativa extract; however, the cellular mechanisms remain ill-defined. TQ-induced cytotoxicity was investigated using canine osteosarcoma (COS31), its cisplatin-resistant variant (COS31/rCDDP), human breast adenocarcinoma (MCF7), human ovarian adenocarcinoma (BG-1) and Madin-Darby canine (MDCK) cell lines. TQ-induced cytotoxicity was determined using a proliferation assay (MTT assay) and apoptosis assays. Effects of TQ on the cell cycle were determined using flow cytometry. COS31/rCDDP resistant cells were the most sensitive cell line to TQ and MDCK cells were the least sensitive. TQ (25 micro M) induced apoptosis of COS31 cells 6 h after treatment and decreased the number of COS31 cells in S-phase and increased cells in G1-phase, indicating cell cycle arrest at G1. These results suggest that TQ kills cancer cells by a process that involves apoptosis and cell cycle arrest. Non-cancerous cells are relatively resistant to TQ.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Benzoquinones / pharmacology*
  • Cell Division / drug effects
  • Cisplatin / pharmacology
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm
  • Flow Cytometry
  • G1 Phase / drug effects
  • Glutathione Transferase / metabolism
  • Humans
  • Tumor Cells, Cultured


  • Antineoplastic Agents
  • Benzoquinones
  • Glutathione Transferase
  • thymoquinone
  • Cisplatin