<p>This study aims to explore the mechanism by which the Translationally controlled tumor protein (TCTP) promotes hyperplasia of the mammary glands (HMG). In this study, the TCTP (Tpt1^flox/flox) and TCTP (Tpt1^KI/KI) gene mice were respectively mated with MMTV-Cre to obtain mice withmammary glands-specific TCTP knockout (TCTP ^cKO) and overexpression (TCTP ^KI). Prepare the HMG animal model by using estrogen combined with progesterone. After the establishment of the TCTP ^cKO and TCTP ^KI mouse models, they are uniformly referred to as HMG ^cKO and HMG ^KI. Hematoxylin and Eosin (H&amp;E) staining and hormone and receptor expression levels were detected. Detect the levels of TCTP, P53, p-AKT, as well as the indicators related to cell apoptosis and cell cycle in the breast tissues of each group. The H&amp;E results showed that compared with the HMG group, the ductal cavity dilation and the number of milk glands in the breast tissue of the HMG ^cKO group were significantly reduced, while the HMG ^KI group exhibited obvious mammary gland hyperplasia. The results showed that compared with the HMG group, the expression levels of Ki67, E₂, FSH, LH, ERα, PR, TCTP, p-AKT, p-BAD, Bcl-2, Cyclin D1, CDK4 and CDK6 in the mammary tissues of the HMG ^cKO group were significantly decreased, while the expression levels of PROG, ERβ, P53, Bax and P27 were significantly increased. In the HMG ^KI group, the opposite results were observed. In our research, it was confirmed that TCTP inhibits cell apoptosis and promotes cell cycle progression by regulating the AKT/P53 signaling pathway, leading to abnormal hyperplasia of the mammary glands. In HMG, by regulating the expression level of TCTP, the effect of treating HMG can be achieved.</p>