Evidence map›Paper›PMID 34567283›Full record

ArticleDisease markers2021

Cancer-Derived Exosomal miR-651 as a Diagnostic Marker Restrains Cisplatin Resistance and Directly Targets ATG3 for Cervical Cancer.

Xiaofan Zhu, Ling Long, He Xiao, Xuan He

Open access · hybridAbstract read
In one paragraph

Article in Disease markers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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  20. Body Weight Is a Valid Predictor of the Long-Term Prognosis of Cervical Cancer.Computational and mathematical methods in medicine · 2022
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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

4 authors at 2 institutions in 1 country.

Xiaofan ZhuDepartment of Obstetrics and Gynecology, Chongqing General Hospital, Chongqing 401147, China.
Ling LongDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Army Medical University, Chongqing 400037, China.
He XiaoCancer Center, Daping Hospital, Army Medical University, Chongqing 400010, China.
Xuan HeCancer Center, Daping Hospital, Army Medical University, Chongqing 400010, China.ORCID https://orcid.org/0000-0002-5505-8416
Army Medical University · CNFirst People's Hospital of Chongqing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCancer-derived exosomes can facilitate drug resistance in cervical cancer. However, the mechanisms remain elusive. Herein, we observed the roles of exosomal miR-651 in cisplatin resistance of cervical cancer.

methodsCirculating miR-651 was detected in cervical cancer and healthy individuals. The diagnostic efficacy was determined. When transfected with miR-651 mimics, cisplatin resistance, apoptosis, and proliferation were assessed. The cancer-derived exosomes were separated and identified. We observed the uptake of PKH67-labeled exosomes by HeLa/S cells. After coculture with exosomes secreted by HeLa/S or HeLa/DDP cells, malignant behaviors were examined in HeLa/S cells. The interactions between ATG3 and miR-651 were validated by dual luciferase report. Biological behaviors were investigated for HeLa/S cells cocultured with exosomes secreted by miR-651 mimic-transfected HeLa/DDP cells.

resultsDownregulated circulating miR-651 was found in cancer subjects than healthy individuals. It possessed high sensitivity and accuracy in diagnosing cervical cancer (AUC = 0.9050). Lower miR-651 expression was confirmed in HeLa/DDP than HeLa/S cells. Forced miR-651 lessened cisplatin resistance and proliferation and elevated apoptosis in HeLa cells. ATG3 was a direct target of miR-651. The exosomes isolated from HeLa cells were rich in CD63, CD9, and CD81 proteins, thereby identifying the isolated exosomes. Exosomes secreted by HeLa/DDP cells can be absorbed by HeLa/S cells. When being cocultured with exosomes secreted by HeLa/DDP cells, malignant behaviors of HeLa/S cells were enhanced, which were ameliorated by miR-651 mimic exosomes.

conclusionOur findings showed that cancer-derived exosomal miR-651 restrained cisplatin resistance and directly targeted ATG3, indicating that exosomal miR-651 could be a therapeutic agent.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisAutophagy-Related ProteinsBiomarkers, TumorCell ProliferationCisplatinExosomesFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsPrognosisTumor Cells, CulturedUbiquitin-Conjugating EnzymesUterine Cervical NeoplasmsAntineoplastic AgentsATG3 protein, humanAutophagy-Related ProteinsBiomarkers, TumorCisplatinMicroRNAsMIRN651 microRNA, humanUbiquitin-Conjugating Enzymes

Identifiers

PMID34567283
PMCPMC8460390
OpenAlexW3199276165

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.