Evidence map›Paper›PMID 30173296›Full record

ArticleBreast cancer research and treatment2018

Extracellular vesicles from triple-negative breast cancer cells promote proliferation and drug resistance in non-tumorigenic breast cells.

Patricia Midori Murobushi Ozawa, Faris Alkhilaiwi, Iglenir João Cavalli, Danielle Malheiros, Enilze Maria de Souza Fonseca Ribeiro, Luciane Regina Cavalli

Open access · hybridAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
4.5field-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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  13. POSTNResearch (Washington, D.C.) · 2025
    Article
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  15. Extracellular vesicles: key mediators inFrontiers in veterinary science · 2025
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13 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

6 authors at 3 institutions in 3 countries.

Patricia Midori Murobushi OzawaDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.ORCID http://orcid.org/0000-0002-7992-143X
Faris AlkhilaiwiFaculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia.
Iglenir João CavalliDepartment of Genetics, Federal University of Paraná, Curitiba, PR, Brazil.
Danielle MalheirosDepartment of Genetics, Federal University of Paraná, Curitiba, PR, Brazil.
Enilze Maria de Souza Fonseca RibeiroDepartment of Genetics, Federal University of Paraná, Curitiba, PR, Brazil.
Luciane Regina CavalliDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA. lrc@georgetown.edu.ORCID http://orcid.org/0000-0001-5619-9037
Universidade Federal do Paraná · BRGeorgetown University · USKing Abdulaziz University · SA

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI STEPHEN W BYERS · 1990 to 2026
$71.5M
Conselho Nacional de Desenvolvimento Científico e Tecnológico 88881.136048/2017-01Fundação Araucária CP 01/16 - PPSUSFundação Araucária PRONEXNCI NIH HHS P30 CA016058NCI NIH HHS P30 CA051008
6 · The paper itself

Abstract

purposeTriple-negative breast cancer (TNBC), an aggressive breast cancer subtype, is genetically heterogeneous which challenges the identification of clinically effective molecular makers. Extracellular vesicles (EVs) are key players in the intercellular signaling communication and have been shown to be involved in tumorigenesis. The main goal of this study was to evaluate the role and mechanisms of EVs derived from TNBC cells in modulating proliferation and cytotoxicity to chemotherapeutic agents in non-tumorigenic breast cells (MCF10A).

methodsEVs were isolated from TNBC cell lines and characterized by nanoparticle tracking analysis, Western blot, and transmission electron microscopy. MCF10A cells were treated with the isolated EVs and evaluated for cell proliferation and cytotoxicity to Docetaxel and Doxorubicin by the MTT and MTS assays, respectively. Gene and miRNA expression profiling was performed in the treated cells to determine expression changes that may be caused by EVs treatment.

resultsMCF10A cells treated with HCC1806-EVs (MCF10A/HCC1806-EVs) showed a significant increase in cell proliferation and resistance to the therapeutic agents tested. No significant effects were observed in the MCF10A cells treated with EVs derived from MDA-MB-231 cells. Gene and miRNA expression profiling revealed 138 genes and 70 miRNAs significantly differentially expressed among the MCF10A/HCC1806-EVs and the untreated MCF10A cells, affecting mostly the PI3K/AKT, MAPK, and HIF1A pathways.

conclusionEVs isolated from the HCC1806 TNBC cells are capable of inducing proliferation and drug resistance on the non-tumorigenic MCF10A breast cells, potentially mediated by changes in genes and miRNAs expression associated with cell proliferation, apoptosis, invasion, and migration.

Indexed as

BreastCell Line, TumorCell ProliferationDrug Resistance, NeoplasmExtracellular VesiclesFemaleGene Expression ProfilingHumansMicroRNAsTriple Negative Breast NeoplasmsMicroRNAsDrug resistanceExosomesGene expressionmiRNA expressionProliferationTNBC

Identifiers

PMID30173296
PMCPMC6245099
OpenAlexW2889110748

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.