Evidence map›Paper›PMID 40335577›Full record

ArticleScientific reports2025

Sinularin induces autophagy-dependent cell death by activating ULK1 and enhancing FOXO3-ATG4A axis in prostate cancer cells.

Xiang-Yu Meng, Yi Li, Ze-Jun Yan, Sha-Zhou Ye, Ke-Jie Wang, Jun-Feng Chen, Rui Yu, Qi Ma

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
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

8 authors.

Xiang-Yu Meng *Ningbo Clinical Research Center for Urological Disease, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Ningbo, 315010, Zhejiang, China.
Yi Li *Department of Urology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, #88 Jiefang Road, Hangzhou, 310009, Zhejiang, China.
Ze-Jun YanNingbo Clinical Research Center for Urological Disease, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Ningbo, 315010, Zhejiang, China.
Sha-Zhou YeNingbo Clinical Research Center for Urological Disease, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Ningbo, 315010, Zhejiang, China.
Ke-Jie WangNingbo Clinical Research Center for Urological Disease, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Ningbo, 315010, Zhejiang, China.
Jun-Feng ChenNingbo Clinical Research Center for Urological Disease, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Ningbo, 315010, Zhejiang, China.
Rui YuDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Health Science Center, Ningbo University, #818 Fenghua Road, Ningbo, 315211, Zhejiang, China. yurui@nbu.edu.cn.
Qi MaNingbo Clinical Research Center for Urological Disease, The First Affiliated Hospital of Ningbo University, #59 Liuting Street, Ningbo, 315010, Zhejiang, China. fyymaqi@nbu.edu.cn.

Funding

Medical and Health Science and Technology Program of Zhejiang Province 2023KY258Natural Science Foundation of Ningbo Municipality 20221JCGY010080Natural Science Foundation of Ningbo Municipality 2023J158Natural Science Foundation of Ningbo Municipality 2024J343Natural Science Foundation of Zhejiang Province LQ20H160008Ningbo Medical Science and Technology Project 2021Y06
6 · The paper itself

Abstract

Sinularin is a natural product extracted from soft coral and is shown to exhibit antitumor effects against multiple human cancers. We previously showed that Sinularin induces apoptotic cell death via stabilizing the FOXO3 protein in prostate cancer cells. In this study, we demonstrated that Sinularin triggers autophagy via two different mechanisms in prostate cancer cells. First, Sinularin reduced the S757 phosphorylation of ULK1 protein, which was mediated by mTOR, leading to ULK1 activation and autophagy initiation. Second, Sinularin enhanced the expression of autophagic protein ATG4A, which is the key regulator in the formation of autophagosome, through a FOXO3-dependent transcriptional mechanism. Next, we identified that ATG4A is a new target gene of the transcription factor FOXO3. Additionally, we also found that Sinularin-induced autophagy promoted survivin degradation and led to cell apoptosis. Taken together, these findings suggest that Sinularin induces prostate cancer cell autophagy by promoting autophagy initiation through activation of ULK1 and formation of autophagosome through the FOXO3-ATG4A pathway.

Indexed as

AutophagyAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsForkhead Box Protein O3Intracellular Signaling Peptides and ProteinsProstatic NeoplasmsApoptosisCell Line, TumorGene Expression Regulation, NeoplasticHumansMalePhosphorylationSignal TransductionAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsForkhead Box Protein O3FOXO3 protein, humanIntracellular Signaling Peptides and ProteinsULK1 protein, humanApoptosisAutophagyFOXO3Prostate cancerSinularin

Identifiers

PMID40335577
PMCPMC12059013

What Socratic holds

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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 Socratic graph.