A Plausible Modeling for Cellular Responding DNA Damage Under Radiotherapys

Abstract

P53, a vital anticancer gene, acts important role in controlling cell cycle arrest and cell apoptosis by regulating the downstream genes and their complicated signal pathways. Under radiotherapy, cell can trigger internal self-defense mechanisms in fighting against genome stresses induced by acute ion radiation (IR). To simulate the cellular responding DNA damage at single cell level, a model for P53 gene networks is proposed under radiotherapy. The model can be used to present the dynamic processes of the double-strand breaks (DSBs) generation and repair, ataxia telangiectasia mutated (ATM) and ARF activation, as well as the oscillations of P53-MDM2 feedback loop in response to acute IR. Especially, the model can predict the plausible outcomes of cellular responding DNA damage versus continuous radiation time.