In this study, researchers from China Medical University in Taiwan investigated the anticancer activity of sulforaphane (SFN), a plant compound present in cruciferous vegetables. The results of their study were published in The American Journal of Chinese Medicine.

• SFN is an isothiocyanate that possesses antitumor and chemopreventive activity. However, previous studies have not yet explored its effects on human colon cancer cells.
• The researchers used HCT 116 cells for their in vitro study.
• They found that SFN can induce cell morphological changes and decrease the cell viability of HCT 116 cells. They used phase-contrast microscopy to observe and photograph these changes.
• They also used flow cytometry and reported the following results:
  • SFN induced G2/M phase arrest and cell apoptosis.
  • SFN also induced the generation of reactive oxygen species (ROS) and Ca2+.
  • SFN decreased mitochondrial membrane potential.
  • SFN increased the activities of caspase-8, -9 and -3 in HCT 116 cells.
• When the researchers performed Western blotting, they observed that SFN increased the expression of cyclin A, cdk 2, cyclin B and Wee1, but decreased the expression of cell division cycle 25 C (Cdc25C) and cdk1, which led to G2/M phase arrest.
• SFN also induced the release of cytochrome c and apoptosis inducing factor (AIF), which was confirmed by confocal microscopy examination.
• They confirmed apoptotic cell death by Annexin V/PI and DAPI staining and DNA gel electrophoresis after HCT 116 cells were treated with SFN.
• They also reported that SFN induced ER stress-associated protein expression.

Based on these findings, the researchers concluded that SFN is a novel anticancer agent that can be used to treat human colon cancer in the future.

Journal Reference:

Liu KC, Shih TY, Kuo CL, Ma YS, Yang JL, Wu PP, Huang YP, Lai KC, Chung JG. SULFORAPHANE INDUCES CELL DEATH THROUGH G2/M PHASE ARREST AND TRIGGERS APOPTOSIS IN HCT 116 HUMAN COLON CANCER CELLS. The American Journal of Chinese Medicine. 2016;44(06):1289–1310. DOI: 10.1142/s0192415x16500725