Evidence map›Paper›PMID 28120942›Full record

ArticleScientific reports2017

The role of miR-26a and miR-30b in HER2+ breast cancer trastuzumab resistance and regulation of the CCNE2 gene.

Eduardo Tormo, Anna Adam-Artigues, Sandra Ballester, Begoña Pineda, Sandra Zazo, Paula González-Alonso, Joan Albanell, Ana Rovira, Federico Rojo, Ana Lluch and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  6. The mechanism of ncRNA in trastuzumab resistance in HER2-positive tumors.Medical oncology (Northwood, London, England) · 2025
    Review
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  13. pPeActa biochimica et biophysica Sinica · 2022
    Article
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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

11 authors at 5 institutions in 1 country.

Eduardo TormoINCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Anna Adam-ArtiguesINCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Sandra BallesterINCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Begoña PinedaINCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Sandra ZazoPathology Department, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain.
Paula González-AlonsoPathology Department, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain.
Joan AlbanellCancer Research Program, IMIM (Hospital del Mar Research Institute), 08003 Barcelona, Spain.
Ana RoviraCancer Research Program, IMIM (Hospital del Mar Research Institute), 08003 Barcelona, Spain.
Federico RojoPathology Department, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain.
Ana LluchINCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Pilar ErolesINCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
INCLIVA Health Research Institute · ESHospital Universitario Fundación Jiménez Díaz · ESHospital Clínico Universitario de Valencia · ESHospital Del Mar · ESMunicipal Institute for Medical Research · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A subset of HER2+ breast cancer patients manifest clinical resistance to trastuzumab. Recently, miR-26a and miR-30b have been identified as trastuzumab response regulators, and their target gene CCNE2 seems to play an important role in resistance to trastuzumab therapy. Cell viability was evaluated in trastuzumab treated HER2+ BT474 wt (sensitive), BT474r (acquired resistance), HCC1954 (innate resistance), and MDA-MB-231 (HER2-) cell lines, and the expression of miR-26a, miR-30b, and their target genes was measured. BT474 wt cell viability decreased by 60% and miR-26a and miR-30b were significantly overexpressed (~3-fold, p = 0.003 and p = 0.002, respectively) after trastuzumab treatment, but no differences were observed in resistant and control cell lines. Overexpression of miR-30b sensitized BT474r cells to trastuzumab (p = 0.01) and CCNE2, was significantly overexpressed after trastuzumab treatment in BT474r cells (p = 0.032), but no significant changes were observed in sensitive cell line. When CCNE2 was silenced BT474r cell sensitivity to trastuzumab increased (p = 0.03). Thus, the molecular mechanism of trastuzumab action in BT474 cell line may be regulated by miR-26a and miR-30b and CCNE2 overexpression might play an important role in acquired trastuzumab resistance in HER2+ breast cancer given that resistance was diminished when CCNE2 was silenced.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsCell CycleCell Line, TumorCell SurvivalCyclinsDown-RegulationDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesFemaleGene SilencingHumansMicroRNAsNeoplasm ProteinsTrastuzumabCCNE2 protein, humanCyclinsErb-b2 Receptor Tyrosine KinasesMicroRNAsMIRN26 microRNA, humanMIRN30b microRNA, humanNeoplasm ProteinsTrastuzumab

Identifiers

PMID28120942
PMCPMC5264595
OpenAlexW2582723358

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.