Evidence map›Paper›PMID 28701793›Full record

ArticleScientific reports2017

The miR-29 transcriptome in endocrine-sensitive and resistant breast cancer cells.

Penn Muluhngwi, Negin Alizadeh-Rad, Stephany L Vittitow, Ted S Kalbfleisch, Carolyn M Klinge

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

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  15. The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021
    Review
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  17. Review
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  19. Article
  20. miRNAs and Long-term Breast Cancer Survival: Evidence from the WHEL Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Article
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

5 authors at 1 institution in 1 country.

Penn MuluhngwiDepartment of Biochemistry & Molecular Genetics, Center for Genetics and Molecular Medicine University of Louisville, Louisville, KY, 40292, USA.
Negin Alizadeh-RadDepartment of Biochemistry & Molecular Genetics, Center for Genetics and Molecular Medicine University of Louisville, Louisville, KY, 40292, USA.
Stephany L VittitowDepartment of Biochemistry & Molecular Genetics, Center for Genetics and Molecular Medicine University of Louisville, Louisville, KY, 40292, USA.
Ted S KalbfleischDepartment of Biochemistry & Molecular Genetics, Center for Genetics and Molecular Medicine University of Louisville, Louisville, KY, 40292, USA.
Carolyn M KlingeDepartment of Biochemistry & Molecular Genetics, Center for Genetics and Molecular Medicine University of Louisville, Louisville, KY, 40292, USA. carolyn.klinge@louisville.edu.ORCID 0000-0002-3358-4378
University of Louisville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant microRNA expression contributes to breast cancer progression and endocrine resistance. We reported that although tamoxifen stimulated miR-29b-1/a transcription in tamoxifen (TAM)-resistant breast cancer cells, ectopic expression of miR-29b-1/a did not drive TAM-resistance in MCF-7 breast cancer cells. However, miR-29b-1/a overexpression significantly repressed TAM-resistant LCC9 cell proliferation, suggesting that miR-29b-1/a is not mediating TAM resistance but acts as a tumor suppressor in TAM-resistant cells. The target genes mediating this tumor suppressor activity were unknown. Here, we identify miR-29b-1 and miR-29a target transcripts in both MCF-7 and LCC9 cells. We find that miR-29b-1 and miR-29a regulate common and unique transcripts in each cell line. The cell-specific and common downregulated genes were characterized using the MetaCore Gene Ontology (GO) enrichment analysis algorithm. LCC9-sepecific miR-29b-1/a-regulated GO processes include oxidative phosphorylation, ATP metabolism, and apoptosis. Extracellular flux analysis of cells transfected with anti- or pre- miR-29a confirmed that miR-29a inhibits mitochondrial bioenergetics in LCC9 cells. qPCR,luciferase reporter assays, and western blot also verified the ATP synthase subunit genes ATP5G1 and ATPIF1 as bone fide miR29b-1/a targets. Our results suggest that miR-29 repression of TAM-resistant breast cancer cell proliferation is mediated in part through repression of genes important in mitochondrial bioenergetics.

Indexed as

Gene Expression Regulation, NeoplasticBiomarkers, TumorBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEstrogen AntagonistsFemaleHumansMicroRNAsMitochondrial ProteinsTamoxifenTranscriptomeTumor Cells, CulturedBiomarkers, TumorEstrogen AntagonistsMicroRNAsMIRN29a microRNA, humanMitochondrial ProteinsTamoxifen

Identifiers

PMID28701793
PMCPMC5507892
OpenAlexW2733368201

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.