Triclosan (Irgasan) is an antibacterial and antifungal agent.

cancer cells with triclosan at the physiologically related concentrations significantly increases the colony number of the cancer cells assessed by tumor formation assay. Triclosan-treated cells have a mesenchymal-like morphology and decrease the cell-to-cell adhesion. Triclosan-treated cells exhibit decreased E-cadherin while significantly up-regulated levels of EMT markers, namely N-cadherin, vimentin, snail and slug. Triclosan may potentiate cancer cells survival in detached condition and motility via the process of EMT[2].

Triclosan plays a pathologic role in promoting tissue fibrogenesis, leading to liver carcinogenesis. It accelerates both HCC development and its long-term effects on liver damage, accompanied by fibrosis and inflammation in mice[1].

CV-1 cells are maintained in DMEM supplemented with 10% FBS, seeded in 96-well plates, and transfected with an expression vector containing a specific nuclear receptor and RXR, along with a luciferase reporter containing the appropriate DNA response element. The assay is first validated with known nuclear receptor ligands as positive controls. For the CAR ligand-binding assay, CV-1 cells are transiently transfected with the expression vector containing the Gal4 DNA-binding domain fused with the ligand-binding domain of murine or human CAR and cotransfected with the luciferase reporter plasmid, mh 100-luc. The day after the transfection, the positive compound of each nuclear receptor or TCS(Triclosan) is added and the cells are incubated for an additional 24 h. The luciferase activities are measured and normalized by β-gal activity.(Only for Reference)