Evidence map›Paper›PMID 31126320›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Inhibition of USP14 enhances the sensitivity of breast cancer to enzalutamide.

Xiaohong Xia, Chuyi Huang, Yuning Liao, Yuan Liu, Jinchan He, Zhiqiang Guo, Lili Jiang, Xuejun Wang, Jinbao Liu, Hongbiao Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
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  11. Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025
    Review
  12. USP14-mediated metabolic competition impairs CD8+ T cell immunosurveillance in hepatocellular carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025
    Review
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2 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 2 countries.

Xiaohong XiaAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Chuyi HuangAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Yuning LiaoAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Yuan LiuAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Jinchan HeAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Zhiqiang GuoAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Lili JiangAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Xuejun WangDivision of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, SD, 57069, USA.
Jinbao LiuAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China. jliu@gzhmu.edu.cn.
Hongbiao HuangAffiliated Cancer Hospital and institute of Guangzhou Medical University; Key Laboratory of Protein Modification and Degradation; State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510095, Guangdong, China. hhb800616@126.com.
State Key Laboratory of Respiratory Disease · CNGuangzhou Medical University · CNUniversity of South Dakota · US

Funding

National Natural Science Foundation of China 81670156, 81872151National Natural Science Foundation of China 81773213
6 · The paper itself

Abstract

backgroundAndrogen receptor (AR) is expressed in approximately 70% of breast tumors. Recent studies increasingly support AR as a potential therapeutic target of AR-positive breast cancer. We have previously reported that deubiquitinase USP14 stabilizes AR proteins by deubiquitination and USP14 inhibition results in inhibition of cell growth and tumor progression in AR-positive prostate cancer and breast cancer. The current study aims to explore the anticancer effect of a treatment combining AR antagonist enzalutamide with USP14 inhibition on breast cancer cells.

methodsThe combining effects of enzalutamide and USP14 inhibition on breast cancer cell proliferation and apoptosis and associated cell signaling were evaluated in vitro and in vivo.

resultsUSP14 inhibition via administration of IU1 or USP14-specific siRNA/shRNA enhanced cell growth inhibition and apoptosis induction by enzalutamide in breast cancer cell lines in vitro and in vivo. Additionally, the combination of enzalutamide with USP14 inhibition/knockdown induced significant downregulation of AR proteins and suppression of AR-related signaling pathways, including Wnt/β-catenin and PI3K/AKT pathways. Moreover, AKT inhibition via MK2206 increased the antiproliferative and proapoptotic effects of enzalutamide+IU1 combined treatment.

conclusionCollectively, our data suggest that USP14 inhibition in combination with enzalutamide represents a potentially new therapeutic strategy for breast cancer.

Indexed as

AnimalsBenzamidesBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDown-RegulationDrug Resistance, NeoplasmDrug SynergismFemaleGene Expression Regulation, NeoplasticHeterocyclic Compounds, 3-RingHumansMCF-7 CellsMiceNitriles1-(1-(4-fluorophenyl)-2,5-dimethylpyrrol-3-yl)-2-pyrrolidin-1-ylethanoneBenzamidesenzalutamideHeterocyclic Compounds, 3-RingMK 2206NitrilesPhenylthiohydantoinPyrrolesPyrrolidinesUbiquitin ThiolesteraseUSP14 protein, humanAndrogen receptorBreast cancerCombination treatmentEnzalutamideUSP14

Identifiers

PMID31126320
PMCPMC6534920
OpenAlexW2947876691

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.