Evidence map›Paper›PMID 35655918›Full record

ArticleDisease markers2022

Extracellular Vesicles Carrying miR-887-3p Promote Breast Cancer Cell Drug Resistance by Targeting BTBD7 and Activating the Notch1/Hes1 Signaling Pathway.

Bing Wang, Yueping Wang, Xuedong Wang, Juan Gu, Wenyong Wu, Huaiguo Wu, Qingping Wang, Daoping Zhou

Open access · hybridAbstract read
In one paragraph

Article in Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  5. Hitting the target: cell signaling pathways modulation by extracellular vesicles.Extracellular vesicles and circulating nucleic acids · 2024
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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

8 authors at 4 institutions in 2 countries.

Bing WangDepartment of Medical Laboratory Science, Fuyang Cancer Hospital, Fuyang, Anhui 236000, China.ORCID https://orcid.org/0000-0001-7320-888X
Yueping WangDepartment of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, China.ORCID https://orcid.org/0000-0002-2668-854X
Xuedong WangDepartment of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, China.ORCID https://orcid.org/0000-0002-7490-9706
Juan GuDepartment of Pathology, The Fifth People's Hospital of Wuxi, Nanjing Medical University, Wuxi, Jiangsu 214000, China.ORCID https://orcid.org/0000-0002-6881-2529
Wenyong WuDepartment of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, China.ORCID https://orcid.org/0000-0002-5564-9152
Huaiguo WuDepartment of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, China.ORCID https://orcid.org/0000-0003-3357-1005
Qingping WangDepartment of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, China.ORCID https://orcid.org/0000-0002-3446-5899
Daoping ZhouDepartment of Medical Laboratory Science, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, China.ORCID https://orcid.org/0000-0002-5210-056X
Anhui Provincial Hospital · CNFuyang Second People's Hospital · CNUniversity of Connecticut · USWuxi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Chemoresistance remains the primary reason threatening the prognosis of breast cancer (BC) patients. Extracellular vesicles (EVs) contribute to chemoresistance by carrying microRNAs (miRNAs). This study investigated the mechanism of miR-887-3p mediated by EVs in BC cell drug resistance. Methods: MDA-MB-231-derived EVs were extracted and identified. BC cells were treated with different concentrations of doxorubicin, cisplatin, and fulvestrant, and the cell survival was evaluated. PKH26-labeled EVs were cocultured with BC cells, and the uptake of EVs was observed. miR-887-3p expression in BC cells and EVs was detected. After silencing miR-887-3p in MDA-MB-231 cells, BC cells were treated with EV-inhi to observe drug resistance. The target gene of miR-887-3p was predicted and verified. The levels of downstream Notch1/Hes1 pathway were detected. Xenograft experiment was conducted to evaluate the effect of EVs on the growth and drug resistance Results: MDA-MB-231-derived EVs enhanced the drug resistance of BC cells. EVs carried miR-887-3p into BC cells. miR-887-3p expression was elevated in BC cells and EVs. miR-887-3p inhibition reduced the drug resistance of BC cells. miR-887-3p targeted BTBD7. Overexpression of BTBD7 partially reversed the drug resistance of BC cells caused by EV treatment. EV treatment increased the level of Notch1/Hes1, and overexpression of BTBD7 decreased the level of Notch1/Hes1. Conclusion: EVs carrying miR-887-3p could target BTBD7 and activate the Notch1/Hes1 signaling pathway, thereby promoting BC cell drug resistance. This study may offer novel insights into BC treatment.

Indexed as

Adaptor Proteins, Signal TransducingBreast NeoplasmsExtracellular VesiclesMicroRNAsDrug Resistance, NeoplasmFemaleHumansReceptor, Notch1Signal TransductionTranscription Factor HES-1Adaptor Proteins, Signal TransducingBTBD7 protein, humanHES1 protein, humanMicroRNAsMIRN887 microRNA, humanNOTCH1 protein, humanReceptor, Notch1Transcription Factor HES-1

Identifiers

PMID35655918
PMCPMC9152417
OpenAlexW4281297418

What OpenQuestion holds

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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.