Evidence mapPaperPMID 40533640Full record

ArticleCell biology and toxicology2025

ADT increases prostate cancer cell invasion via altering AR/SALL4/SOX2-OCT4 stem cell signaling.

Changcheng Guo, Aimaitiaji Kadier, Zhijin Zhang, Shiyu Mao, Bin Yang, Junhua Zheng, Xudong Yao

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Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

  1. Review
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4 · The record

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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

7 authors.

Changcheng Guo *Department of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Aimaitiaji Kadier *Department of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Zhijin Zhang *Department of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Shiyu MaoDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Bin YangDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Junhua ZhengDepartment of Urology, Renji Hospital, School of Medicine in Shanghai Jiao Tong University, Shanghai, 200072, China.
Xudong YaoDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. yaoxudong1967@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early studies indicated that the androgen-deprivation-therapy with antiandrogen Enzalutamide (Enz) could increase prostate cancer patients' survival by an average of 4.8 months. Yet Enz might also have some adverse effects via increasing the prostate cancer (PCa) cell invasion. Here we found Enz treatment could increase SALL4 expression to increase the cancer stem cells-like (CSC-like) population that resulted in increasing the PCa cell invasion. Mechanism dissection revealed that Enz could function via androgen receptor (AR) to transcriptionally regulate the SALL4 expression via direct binding on the SALL4 5'-promoter. The consequences of such Enz/AR/SALL4 axis could upregulate the SOX2-OCT4 expression to increase the CSC-like population and the PCa cells invasion. Together, results from multiple in vitro and in vivo experiments all conclude that Enz may induce the adverse effect of increasing PCa cells invasion via altering the AR/SALL4/SOX2-OCT4 signaling to increase the CSC-like population, and targeting SALL4 may decrease this adverse effect for further suppress the PCa progression.

Indexed as

Androgen AntagonistsNeoplastic Stem CellsOctamer Transcription Factor-3Prostatic NeoplasmsReceptors, AndrogenTranscription FactorsAnimalsBenzamidesCell Line, TumorGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm InvasivenessNitrilesAndrogen AntagonistsAR protein, humanBenzamidesenzalutamideNitrilesOctamer Transcription Factor-3PhenylthiohydantoinPOU5F1 protein, humanReceptors, AndrogenSALL4 protein, humanSOX2 protein, humanSOXB1 Transcription FactorsTranscription FactorsCancer stem cells-likeDrug resistanceProstate cancerSALL4

Identifiers

PMID40533640
PMCPMC12176959

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.