Evidence map›Paper›PMID 30975171›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Inhibition of EGFR signaling with Spautin-1 represents a novel therapeutics for prostate cancer.

Yuning Liao, Zhiqiang Guo, Xiaohong Xia, Yuan Liu, Chuyi Huang, 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 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 100 citations in OpenAlex.

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  11. Optimizing Human Cell-Free System for Efficient Protein Production.Journal of microbiology and biotechnology · 2025
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  17. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
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  20. Article

4 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

9 authors at 3 institutions in 2 countries.

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, 511436, 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, 511436, Guangdong, China.
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, 511436, 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, 511436, 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, 511436, 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, 511436, 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, 511436, 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, 511436, Guangdong, China. hhb800616@126.com.
Guangzhou Medical University · CNState Key Laboratory of Respiratory Disease · CNUniversity of South Dakota · US

Funding

the National Natural Science Foundation of China 81472390the National Natural Science Foundation of China 81773213the National Natural Science Foundation of China 81872151
6 · The paper itself

Abstract

backgroundProstate cancer (PCa) remains a challenge worldwide. Due to the development of castration-resistance, traditional first-line androgen deprivation therapy (ADT) became powerlessness. Epidermal growth factor receptor (EGFR) is a well characterized therapeutic target to treat colorectal carcinoma and non-small cell lung cancer. Increasing studies have unraveled the significance of EGFR and its downstream signaling in the progression of castration-resistant PCa.

methodMTS, colony formation and Edu staining assays were used to analyze the cell proliferation of PCa cells. Flow cytometry was used to analyze PCa cell cycle distribution and cell apoptosis. Western blot was used to measure the expression of key proteins associated with cell cycle progression, apoptosis and EGFR signaling pathways. Transfection of exogenous small interfering RNA (siRNA) or plasmid was used to intervene specific gene expression. Nude mouse model was employed to test the in vivo effect of Spautin-1.

resultsThe current study reveals that Spautin-1, a known inhibitor of ubiquitin-specific peptidase 10 (USP10) and USP13, inhibits EGFR phosphorylation and the activation of its downstream signaling. Inhibition of EGFR signaling induced by Spautin-1 leads to cell cycle arrest and apoptosis of PCa in a USP10/USP13 independent manner. The application of Spautin-1 reduces the expression of glucose transporter 1 (Glut1) and dramatically induces cell death under glucose deprivation condition. In vivo experiments show a potent anti-tumor effect of Spautin-1 alone and in combination with Enzalutamide.

conclusionThis study demonstrates the therapeutic potential of EGFR signaling inhibition by the use of Spautin-1 for PCa treatment.

Indexed as

AnimalsApoptosisAutophagyBenzamidesBenzylaminesBiomarkers, TumorCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin D1Disease Models, AnimalErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticGlucoseGlucose Transporter Type 1BenzamidesBenzylaminesBiomarkers, TumorCyclin D1EGFR protein, humanenzalutamideErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGlucoseGlucose Transporter Type 1JNK Mitogen-Activated Protein KinasesNitrilesPhenylthiohydantoinQuinazolinesspautin-1ApoptosisEGFRGlut1Prostate cancerSpautin-1

Identifiers

PMID30975171
PMCPMC6460657
OpenAlexW2938931338

What OpenQuestion holds

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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.