Each stage of cell growth is inseparable from the protein-protein interactions. It is of great significance in studying the function of the cell cycle, regulatory mechanism, and relationships among the proteins involved in the regulation in biological engineering and other fields. This paper studies the function, principle, and self-repairing mechanisms based on the intracellular protein p53 when DNA is damaged by ionizing radiation. We introduce more regulating factors for the proteins to build the networks based on the existing one and simulate a more comprehensive cell cycle progression. Then we analyze the anti-interference and self-repairing system of the regulatory networks using the complex network theory and cell cycle regulation. Numerical simulation results and experimental data show: (1) The protein network shows a stable condition when it suffers a small disturbance, while it shows a poor stability when facing deliberate attack; (2) whether the damaged DNA can be repaired depends on the dynamic behavior of p53 protein, i.e., p53 can transmit the damage signal to the cell cycle regulatory factors through the signal transduction pathway to induce the cell cycle arrest so as to complete the self-repairing processes in the case of the low-damage and the medium-damage. When DNA comes to face the high-damage and the excess-damage, the concentration of p53 shows a periodic oscillation behavior and it can induce apoptosis.