- Proliferative and Apoptotic Signaling in Oral Cancer
Apoptosis is a regulated event of cell death, i.e., a morphologically and biochemically distinct mode of cell death that occurs during embryogenesis, carcinogenesis, cancer treatment, or immune reactions, as well as in cell proliferation (Khan et al., 2010a, 2012; Sah et al., 2006). It is an important regulated process that counterbalances the cells produced due to cell division and complements differentiation in the overall tissue homeostatic mechanisms. The realization that apoptosis is a genedirected program has had profound implications for our understanding of developmental biology and tissue homeostasis, for it implies that cell numbers can be regulated by factors that influence cell survival as well as those that control proliferation and differentiation. Several lines of evidence link apoptosis to proliferation. A number of dominant oncogenes have a dual role: they can induce both proliferation and apoptosis. As somatic cells proliferate, the cell cycle progression is regulated by positive and negative signals. Cell cycle genes such as p53, Rb, and E2F have been shown to participate in both the cell cycle and apoptosis (Cao et al., 1992; Khan and Bisen, 2013). Thus, the balance between apoptosis and proliferation must be strictly maintained to sustain tissue homeostasis.