Evidence map›Paper›PMID 29339789›Full record

ArticleScientific reports2018

Exosome-mediated breast cancer chemoresistance via miR-155 transfer.

Juliana Carvalho Santos, Natália da Silva Lima, Luis Otavio Sarian, Ander Matheu, Marcelo Lima Ribeiro, Sophie Françoise Mauricette Derchain

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 1 pooled it
16.6field-weighted citation impact, top 1% 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

207 citing papers in PubMed, 1 synthesis or guideline pooled it, 329 citations in OpenAlex.

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  19. Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025
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147 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 2 countries.

Juliana Carvalho SantosWomen's Health Hospital "Prof Dr José Aristodemo Pinotti" (CAISM), State University of Campinas (UNICAMP), Campinas, SP, Brazil. santos.j.c@outlook.com.
Natália da Silva LimaClinical Pharmacology and Gastroenterology Unit, São Francisco University, São Francisco University, Bragança Paulista, SP, Brazil.
Luis Otavio SarianWomen's Health Hospital "Prof Dr José Aristodemo Pinotti" (CAISM), State University of Campinas (UNICAMP), Campinas, SP, Brazil.
Ander MatheuCellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Marcelo Lima RibeiroClinical Pharmacology and Gastroenterology Unit, São Francisco University, São Francisco University, Bragança Paulista, SP, Brazil. marcelo.ribeiro@usf.edu.br.ORCID http://orcid.org/0000-0003-4529-7832
Sophie Françoise Mauricette DerchainWomen's Health Hospital "Prof Dr José Aristodemo Pinotti" (CAISM), State University of Campinas (UNICAMP), Campinas, SP, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BRUniversidade São Francisco · BRBiogipuzkoa Health Research Institute · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer remains the most prevalent cause of cancer mortality in woman worldwide due to the metastatic process and therapy resistance. Resistance against cancer therapy is partially attributed to cancer stem cells (CSCs). These cells arise from epithelial cells undergoing epithelial-to-mesenchymal transition (EMT) and might be responsible for tumor recurrence. In this study, we reported the relevance of miR-155 upregulation in chemoresistant cells associated with EMT. Notably, we found miR-155 induction in exosomes isolated from CSCs and resistant cells, followed by resistant cells' exosome transfer to the recipient sensitive cells. Functionally, miR-155 mimic assay showed an enrichment in miR-155 from exosome concomitant with miR-155 exosome transfer to breast cancer cells. In parallel to these effects, we also observed EMT change in miR-155 transfected cells. The chemoresistance phenotype transfer to sensitive cells and the migration capability was analyzed by MTT and scratch assays and our results suggest that exosomes may intermediate resistance and migration capacity to sensitive cells partly through exosome transfer of miR-155. Taken together, our findings establish the significance of exosome-mediate miR-155 chemoresistance in breast cancer cells, with implications for targeting miR-155 signaling as a possible therapeutic strategy.

Indexed as

Drug Resistance, NeoplasmAntagomirsAntineoplastic AgentsBreast NeoplasmsCadherinsCell MovementCell SurvivalEpithelial-Mesenchymal TransitionExosomesFemaleHumansMicroRNAsNeoplastic Stem CellsPolycomb Repressive Complex 1SOX9 Transcription FactorUp-RegulationAntagomirsAntineoplastic AgentsBMI1 protein, humanCadherinsMicroRNAsMIRN155 microRNA, humanPolycomb Repressive Complex 1SOX9 protein, humanSOX9 Transcription Factor

Identifiers

PMID29339789
PMCPMC5770414
OpenAlexW2782752196

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.