Biochemistry Seminar
"TP53AIP1 Induce Autophagy via the AKT/mTor Signaling Pathway in the Breast Cancer Cells"
Zoom Link:
https://notredame.zoom.us/j/96578936757?pwd=NbZCP9I2QyXaeCGmB7QNkIaMkVYVVX.1
Meeting ID: 965 7893 6757
Passcode: 961439
Abstract
TP53AIP1 (Tumor Protein p53 Regulated Apoptosis Inducing Protein 1) plays a crucial role in regulating cellular responses to stress, including in apoptosis and autophagy. In this study, the authors investigated the role of TP53AIP1 in the progression of breast cancer, in addition to exploring the underlying molecular mechanisms. They used different experimental techniques including CCK8 assays, wound healing assays, RT-qPCR, flow cytometry, western blotting etc. The results demonstrate that TP53AIP1 induces autophagy in breast cancer cell lines through the inactivation of the AKT/mTOR signaling pathway. Specifically, TP53AIP1 expression inhibits the phosphorylation of AKT, which subsequently inactivates mTOR, promoting autophagic flux. Inhibition of the AKT/mTOR pathway significantly attenuates TP53AIP1-induced autophagy, confirming the involvement of this signaling pathway. Furthermore, they showed that autophagy induced by TP53AIP1 contributes to enhanced cell survival under nutrient deprivation, suggesting a potential mechanism by which breast cancer cells adapt to hostile tumor microenvironments. The findings provide new insights into the molecular interplay between TP53AIP1 and autophagy, offering potential therapeutic avenues for targeting the AKT/mTOR pathway in breast cancer treatment.
Shutian Liu, Ting Xu, Xi Chen, Li Tang, Longjiang Li, Li Zhang, Yongqiang Yang & Jiayi Huang