Evidence map›Paper›PMID 37356089›Full record

ArticleMolecular oncology2023

Synergistic inhibition of NUDT21 by secretory S100A11 and exosomal miR-487a-5p promotes melanoma oligo- to poly-metastatic progression.

Bin Zeng, Yuting Chen, Hao Chen, Qiting Zhao, Zhiwei Sun, Doudou Liu, Xiaoshuang Li, Yuhan Zhang, Jianyu Wang, H Rosie Xing

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  6. Multi-stage mechanisms of tumor metastasis and therapeutic strategies.Signal transduction and targeted therapy · 2024
    Review
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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.

Bin ZengInstitute of Life Sciences, Chongqing Medical University, China.
Yuting ChenState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, China.
Hao ChenState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, China.
Qiting ZhaoInstitute of Life Sciences, Chongqing Medical University, China.
Zhiwei SunInstitute of Life Sciences, Chongqing Medical University, China.
Doudou LiuState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, China.
Xiaoshuang LiState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, China.
Yuhan ZhangState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, China.
Jianyu WangInstitute of Life Sciences, Chongqing Medical University, China.ORCID 0000-0002-6338-5898
H Rosie XingState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, China.ORCID 0000-0001-5894-0837
Chongqing University · CNChongqing Medical University · CNZen-Noh (Japan) · JP

Funding

National Natural Science Fund of China 82073277National Natural Science Fund of China 82173247Project of Chongqing Natural Science Foundation Innovation and Development Fund (Municipal Education Commission) CSTB2022NS CQ-LZX0023Science and Technology Project Affiliated to the Education Department of Chongqing KJQN202100404
6 · The paper itself

Abstract

Although early diagnosis and therapeutic advances have transformed the living quality and outcome of cancer patients, the poor prognosis for metastatic patients has not been significantly improved. Mechanisms underlying the complexity of metastasis cannot be simply determined by the straightforward 'cause-and-effect relationships'. We have developed a 'dry-lab-driven knowledge discovery and wet-lab validation' approach to embrace the complexity of cancer and metastasis. We have revealed for the first time that polymetastatic (POL) melanoma cells can utilize both the secretory protein pathway (S100A11-Sec23a) and the exosomal crosstalk (miR-487a-5p) to transfer their 'polymetastatic competency' to the oligometastatic (OL) melanoma cells, via synergistic co-targeting of the tumor-suppressor Nudt21. The downstream deregulated glycolysis was verified to regulate metastatic colonization efficiency. Further, two gene sets conferring independent prognosis in melanoma were identified, which have the potential for clinical translation and merit future clinical validation.

Indexed as

ExosomesMelanomaMicroRNAsBiological TransportCell Line, TumorCell ProliferationCleavage And Polyadenylation Specificity FactorGene Expression Regulation, NeoplasticHumansS100 ProteinsCleavage And Polyadenylation Specificity FactorMicroRNAsNudt21 protein, humanS100A11 protein, humanS100 ProteinsexosomeglycolysismiR-487a-5pNudt21S100A11Sec23a

Identifiers

PMID37356089
PMCPMC10701767
OpenAlexW4381946647

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.