Evidence map›Paper›PMID 35920704›Full record

ArticleAutophagy2023

TOLLIP-mediated autophagic degradation pathway links the VCP-TMEM63A-DERL1 signaling axis to triple-negative breast cancer progression.

Tai-Mei Zhang, Li Liao, Shao-Ying Yang, Min-Ying Huang, Yin-Ling Zhang, Ling Deng, Shu-Yuan Hu, Fan Yang, Fang-Lin Zhang, Zhi-Min Shao and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.0field-weighted citation impact, top 2% of its field
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

37 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  10. Garciniagifolone A, derived fromFrontiers in cell and developmental biology · 2026
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  20. VCP downstream metabolite glycerol-3-phosphate (G3P) inhibits CD8Signal transduction and targeted therapy · 2025
    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

11 authors at 2 institutions in 1 country.

Tai-Mei ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Li LiaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Shao-Ying YangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Min-Ying HuangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Yin-Ling ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Ling DengFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Shu-Yuan HuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Fan YangDepartment of Breast Surgery, Shanghai Medical College, Fudan University, Shanghai, Yangpu, China.
Fang-Lin ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.
Zhi-Min ShaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.ORCID 0000-0003-2967-0369
Da-Qiang LiFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai Yangpu, China.ORCID 0000-0002-5113-2332
Shanghai Medical College of Fudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is the most challenging breast cancer subtype to treat due to the lack of effective targeted therapies. Transmembrane (TMEM) proteins represent attractive drug targets for cancer therapy, but biological functions of most members of the TMEM family remain unknown. Here, we report for the first time that TMEM63A (transmembrane protein 63A), a poorly characterized TMEM protein with unknown functions in human cancer, functions as a novel oncogene to promote TNBC cell proliferation, migration, and invasion

Indexed as

Triple Negative Breast NeoplasmsApoptosis Regulatory ProteinsAutophagyEndoplasmic Reticulum-Associated DegradationHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsSignal TransductionValosin Containing ProteinApoptosis Regulatory ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsTOLLIP protein, humanValosin Containing ProteinVCP protein, humanMacroautophagic degradationproteostasisselective autophagy receptortransmembrane proteintriple-negative breast cancer

Identifiers

PMID35920704
PMCPMC9980475
OpenAlexW4289550200

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.