Evidence map›Paper›PMID 32129945›Full record

ArticleJournal of cellular and molecular medicine2020

Potent USP10/13 antagonist spautin-1 suppresses melanoma growth via ROS-mediated DNA damage and exhibits synergy with cisplatin.

Jia Guo, JiangLing Zhang, Long Liang, Nian Liu, Min Qi, Shuang Zhao, Juan Su, Jing Liu, Cong Peng, Xiang Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. USP10-mediated deubiquitination and activation ofActa pharmaceutica Sinica. B · 2026
    Article
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  11. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
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  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. USP13: Multiple Functions and Target Inhibition.Frontiers in cell and developmental biology · 2022
    Review
  19. Article
  20. Role of USP13 in physiology and diseases.Frontiers in molecular biosciences · 2022
    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

11 authors at 1 institution in 1 country.

Jia GuoDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
JiangLing ZhangDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Long LiangDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Nian LiuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Min QiDepartment of Plastic and Cosmetic Surgery, Xiangya Hospital, Central South University, Changsha, China.
Shuang ZhaoDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Juan SuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Jing LiuMolecular Biology Research Center and Center for Medical Genetics, Central South University, Changsha, China.ORCID 0000-0002-9317-774X
Cong PengDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Xiang ChenDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.
Hong LiuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, China.ORCID 0000-0001-9976-2985
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma is one of the most invasive tumours. However, effective therapeutic strategies are limited, and overall survival rates remain low. By utilizing transcriptomic profiling, tissue array and molecular biology, we revealed that two key ubiquitin-specific proteases (USPs), ubiquitin-specific peptidase10 (USP10) and ubiquitin-specific peptidase10 (USP13), were significantly elevated in melanoma at the mRNA and protein levels. Spautin-1 has been reported as a USP10 and USP13 antagonist, and we demonstrated that spautin-1 has potent anti-tumour effects as reflected by MTS and the colony formation assays in various melanoma cell lines without cytotoxic effects in HaCaT and JB6 cell lines. Mechanistically, we identified apoptosis and ROS-mediated DNA damage as critical mechanisms underlying the spautin-1-mediated anti-tumour effect by utilizing transcriptomics, qRT-PCR validation, flow cytometry, Western blotting and immunofluorescence staining. Importantly, by screening spautin-1 with targeted or chemotherapeutic drugs, we showed that spautin-1 exhibited synergy with cisplatin in the treatment of melanoma. Pre-clinically, we demonstrated that spautin-1 significantly attenuated tumour growth in a cell line-derived xenograft mouse model, and its anti-tumour effect was further enhanced by cotreatment with cisplatin. Taken together, our study revealed a novel molecular mechanism of spautin-1 effecting in melanoma and identified a potential therapeutic strategy in treatment of melanoma patients.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBenzylaminesCell Line, TumorCisplatinCutaneous Malignant MelanomaDNA DamageDrug SynergismGene Expression Regulation, NeoplasticHumansMelanomaMiceQuinazolinesReactive Oxygen SpeciesSkin NeoplasmsAntineoplastic AgentsBenzylaminesCisplatinQuinazolinesReactive Oxygen Speciesspautin-1Ubiquitin-Specific ProteasesUbiquitin ThiolesteraseUSP10 protein, humanUSP13 protein, humancombination therapyDNA damagemalignant melanomaROSspautin-1

Identifiers

PMID32129945
PMCPMC7171391
OpenAlexW3009911520

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.