Evidence map›Paper›PMID 40198519›Full record

ArticleMolecular and cellular biochemistry2025

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

Zhaofeng Li, Xueyu Li, Han Yang, Meixiang Huang, Zhu Liu, Zongliang Zhang, Kai Zhao, Xinbao Yin, Guanqun Zhu, Yulian Zhang and 6 more

Abstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Zhaofeng Li *Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Xueyu Li *Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Han YangDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Meixiang HuangHospital-Acquired Infection Control Department, Qingdao Central Hospital, Qingdao, Shandong, China.
Zhu LiuLingzhushan Street Community Health Service Center (Lingzhushan Street Health Center), Huangdao District, Qingdao, China.
Zongliang ZhangDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Kai ZhaoDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Xinbao YinDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Guanqun ZhuDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Yulian ZhangDepartment of Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Zhenlin WangDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Qinglei WangDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Zaiqing JiangDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Suofei ZhangDepartment of Urology, Laixi People's Hospital, Yantai, Shangdong, China.
Tianzhen HeInstitute of Special Environmental Medicine, Nantong University, Nantong, 226019, China. sailing198562@ntu.edu.cn.
Ke WangDepartment of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China. wangke@qdu.edu.cn.

Funding

Large Instruments Open Foundation of Nantong University KFJN2375National Natural Science Foundation of China 31971191National Natural Science Foundation of China 82100557National Natural Science Foundation of China 82200759
6 · The paper itself

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.

Indexed as

Cell CycleGene Expression Regulation, NeoplasticNeoplasm ProteinsProstatic NeoplasmsTumor Suppressor Protein p53Cell Line, TumorCell ProliferationDisease ProgressionHumansMaleNeoplasm ProteinsTP53 protein, humanTumor Suppressor Protein p53Cell cycle dysregulationInvasionP53ProliferationProstate adenocarcinomaTOR1 AIP1

Identifiers

PMID40198519
PMCPMC12263815

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.