Regulation of the AKT/P53 signaling pathway by translated control tumor protein inhibits apoptosis and promotes hyperplasia of the mammary glands.

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&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&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, E(2), 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.