# TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

## TL;DR

This study shows that TOR1 AIP1 interacts with p53 to stop prostate cancer cell growth, suggesting it could be a new treatment target.

## Contribution

The study identifies TOR1 AIP1 as a novel regulator of p53 stability and tumor suppression in prostate cancer.

## Key findings

- TOR1 AIP1 is low in prostate cancer and correlates with worse survival outcomes.
- TOR1 AIP1 stabilizes p53 and inhibits tumor proliferation and invasion.
- Upregulation of TOR1 AIP1 arrests the cell cycle in the S phase.

## Abstract

The cell cycle mechanism is an integration point where information is sent through an upstream signaling network, making it a potential target for cancer diagnosis and treatment. The LAP1 protein, encoded by the Tor1aip1 gene, is required to maintain the shape of the nuclear envelope and the progression of the cell cycle. The aim of this study was to determine the role of Tor1aip1 gene in PRAD development and its mechanism. We analyzed the expression and survival data of TOR1 AIP1 in PRAD patients in the TCGA database and verified the low expression of TOR1 AIP1 in prostate cancer by qPCR, western blot and immunohistology, which was correlated with the tumor stage and survival prognosis of PRAD. In addition, lentiviral vectors were used to mediate the up-regulation or down-regulation of TOR1 AIP1 expression in prostate cancer cells, and the effects of TOR1 AIP1 on tumor proliferation and related signaling pathways were investigated by cell counting kit- 8, colony formation assay, transwell assay, western blot, and flow cytometry. As a result, we found that TOR1 AIP1 enhances protein stability of p53 by directly interacting with p53, consequently inhibited tumor proliferation and invasion by inducing the cell cycle to be arrested in the S phase. Therefore, TOR1 AIP1 represents a promising therapeutic target in PRAD due to its ability to stabilize p53 and enhance its tumor-suppressive functions. Future studies should focus on elucidating its mechanisms, developing targeted therapies, and exploring its clinical potential in combination with existing treatments. By advancing our understanding of TOR1 AIP1, we may unlock new strategies for improving outcomes in PRAD patients.

The online version contains supplementary material available at 10.1007/s11010-025-05276-1.