Evidence map›Paper›PMID 40394639›Full record

ArticleJournal of translational medicine2025

AP5Z1 affects hepatocellular carcinoma growth and autophagy by regulating PTEN ubiquitination and modulating the PI3K/Akt/mTOR pathway.

Zhipeng Quan, Bo Peng, Kai Hu, Lixing Liang, Mingjiang Liu, Lijuan Liao, Shilian Chen, Jing Qin, Songqing He, Zeyuan Li

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

7 citing papers in PubMed.

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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

10 authors.

Zhipeng Quan *Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China.ORCID 0000-0002-1079-5666
Bo Peng *Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Kai HuGuangxi Key Laboratory of Immunology and Metabolism for Liver Diseases, Nanning, Guangxi, 530021, China.
Lixing LiangGuangxi Key Laboratory of Immunology and Metabolism for Liver Diseases, Nanning, Guangxi, 530021, China.
Mingjiang LiuDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Lijuan LiaoDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Shilian ChenDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Jing QinGuangxi Key Laboratory of Immunology and Metabolism for Liver Diseases, Nanning, Guangxi, 530021, China.
Songqing HeDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China. dr_hesongqing@163.com.
Zeyuan LiDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, NO 6 Shuangyong Road, Nanning, Guangxi, 530021, China. lizeyuan03@126.com.ORCID 0000-0001-5861-8119

Funding

Innovation Project of Guangxi Graduate Education YCBZ2024131Joint Project on Regional High-Incidence Diseases Research of Guangxi Natural Science Foundation 2023GXNSFAA026001The 111 Project D17011Youth Science Foundation of Guangxi Medical University GXMUYSF202414
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is a leading cause of cancer death worldwide, with high incidence and mortality rates, and the number of cases is expected to increase by 2030. Understanding the molecular mechanisms of HCC and identifying new therapeutic targets and biomarkers for HCC are crucial.

methodsIn this study, we examined adaptor-related protein complex 5 subunit ζ1 (AP5Z1) expression in liver cancer and nearby noncancerous tissues to explore its effects on HCC cell growth, death, and autophagy. The functional and molecular mechanisms of AP5Z1 were studied using clinical sample analysis, Western blot (WB), immunohistochemistry (IHC), quantitative reverse-transcription polymerase chain reaction (qRT‒PCR), coimmunoprecipitation (Co-IP), cell proliferation assays, flow cytometry (FCM), autophagy assays, electron microscopy, mass spectrometry (MS), transcriptome analysis, and animal model experiments.

resultsAP5Z1 expression was notably higher in HCC tissues than in normal tissues and was linked to a poor prognosis. The results of both in vitro and in vivo studies revealed that AP5Z1 promoted HCC cell growth and reduced apoptosis. In addition, AP5Z1 regulates cellular autophagy by ubiquitinating the phosphatase and tensin homolog (PTEN) protein and modulating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway.

conclusionsAP5Z1 influences autophagy and apoptosis in HCC cells by interacting with PTEN to modulate the PI3K/Akt/mTOR pathway. This gene might promote PTEN ubiquitination and degradation by recruiting tripartite motif-containing protein 21 (TRIM21), making it a potential biomarker for diagnosing and predicting the outcome of HCC as well as a target for new treatment strategies.

Indexed as

AutophagyCarcinoma, HepatocellularLiver NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTOR Serine-Threonine KinasesUbiquitinationAnimalsApoptosisCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine KinasesAP5Z1ApoptosisAutophagyHepatocellular carcinomaPI3K/Akt/mTOR signalling pathwayPTENTRIM21Ubiquitination

Identifiers

PMID40394639
PMCPMC12090622

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.