The Role of p53 in Carcinogenesis and Apoptosis in Oral Tissues

Abstract

Reactive oxygen species (ROS) cause DNA double-strand or single-strand breaks. ROS form one of the main causes of DNA damage. Environmental factors as well as host factors increase ROS. The volatile sulfur compounds in the oral cavity, especially oral malodorous compounds, are the most probable producers of ROS. The functions of p53 involve causing p53-dependent apoptosis, repairing DNA-strand errors and arresting the cell cycle for DNA repair. A signal network reacting to DNA or genomic damage selects either apoptosis or the repair of DNA breaks after the cellular DNA or genome is damaged. The network involves the checkpoints: p53, Ataxia-telangiectasia and Rad3-related (ATR), and Ataxia-telangiectasia mutated (ATM) protein kinase have important roles. The signal network works together with the cell cycle. Checkpoints in the network hold the cell cycle at a certain point. Genotoxicity, in which checkpoint kinase 1 and 2 also have important roles, controls the network, including the checkpoints, indirectly. There are three groups of checkpoints: cell-cycle checkpoints (DNA-damage checkpoints), DNA-replication checkpoints, and the spindle checkpoint. These checkpoints detect DNA damage and then promote either DNA repair or cell death. Because of this system the cell preserves genomic integrity. In other words, the cell and/or the host can eliminate genomic error from the host.