Evidence map›Paper›PMID 41565619›Full record

ArticleCell death & disease2026

Positive feedback regulation between USP8 and Hippo/YAP axis drives triple-negative breast cancer progression.

Xin Li, Penghe Yang, Tianshi Wang, Peng Su, Chenmiao Zhang, Shen Fangyu, Huijie Yang, Jian Zhu, Xiaodong Tan, Ting Zhuang

Abstract read
In one paragraph

Article in Cell death & disease, 2026. 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

10 authors.

Xin Li *Xinxiang Key Laboratory of Tumor Migration and Invasion Precision Medicine, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan Province, PR China.ORCID http://orcid.org/0009-0007-3315-3408
Penghe Yang *Xinxiang Key Laboratory of Tumor Migration and Invasion Precision Medicine, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan Province, PR China.
Tianshi Wang *Department of General Surgery, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, PR China.
Peng Su *Department of Pathology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, PR China.ORCID http://orcid.org/0000-0002-7000-0474
Chenmiao ZhangXinxiang Key Laboratory of Tumor Migration and Invasion Precision Medicine, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan Province, PR China.
Shen FangyuXinxiang Key Laboratory of Tumor Migration and Invasion Precision Medicine, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan Province, PR China.
Huijie YangXinxiang Key Laboratory of Tumor Migration and Invasion Precision Medicine, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan Province, PR China.
Jian ZhuDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, PR China. zhujian1204@yahoo.com.ORCID http://orcid.org/0000-0003-3596-4339
Xiaodong TanDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, PR China. tanxdcmu@163.com.ORCID http://orcid.org/0000-0003-0862-1306
Ting ZhuangXinxiang Key Laboratory of Tumor Migration and Invasion Precision Medicine, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan Province, PR China. 77090993@qq.com.ORCID http://orcid.org/0000-0002-6308-1253

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hyper-activation of the Hippo/YAP axis was observed in triple-negative breast cancer (TNBC), which was crucial for tumor progression. The over-activation of YAP in TNBC remains unexplained, despite the continued functionality of the inhibitory phospho-cascade. Recently, studies revealed that the ubiquitin modifications of YAP also play important roles in the Hippo/YAP axis and cancer progression. In order to understand the potential mechanisms of ubiquitination and deubiquitination process in YAP function, we carried out siRNA screening for critical deubiquitinases in TNBC. Via the deubiquitinases (DUB) library, we identified Ubiquitin Specific Peptidase 8 (USP8) as an important effector in YAP function and TNBC progression. Inhibition of USP8 hampered TNBC progression via Hippo signaling. Clinical data revealed that USP8 expression correlated with YAP protein level and poor survival in TNBC patients. Biochemical evaluations revealed that USP8 has the ability to connect with YAP and suppress K48-linked polyubiquitination, thereby enhancing the stability of YAP. Interestingly, YAP directly binds to the USP8 promoter region, enhancing its transcription in TNBC. Our study revealed a forward feedback loop between USP8 and Hippo signaling in TNBC, indicating USP8 as a potential therapeutic drug targets in TNBC.

Indexed as

Adaptor Proteins, Signal TransducingEndopeptidasesFeedback, PhysiologicalPhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsTriple Negative Breast NeoplasmsUbiquitin ThiolesteraseAnimalsCell Line, TumorDisease ProgressionEndosomal Sorting Complexes Required for TransportFemaleGene Expression Regulation, NeoplasticHippo Signaling PathwayHumansAdaptor Proteins, Signal TransducingEndopeptidasesEndosomal Sorting Complexes Required for TransportPhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsUbiquitin ThiolesteraseUSP8 protein, humanYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID41565619
PMCPMC12830590

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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.