Evidence map›Paper›PMID 27562865›Full record

ArticleJournal of cancer research and clinical oncology2016

MiR-26a and miR-138 block the G1/S transition by targeting the cell cycle regulating network in prostate cancer cells.

Kati Erdmann, Knut Kaulke, Christiane Rieger, Karsten Salomo, Manfred P Wirth, Susanne Fuessel

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

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  10. Role of hydrogen sulfide donors in cancer development and progression.International journal of biological sciences · 2021
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  16. Pivotal role of microRNA-138 in human cancers.American journal of cancer research · 2019
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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

6 authors at 2 institutions in 1 country.

Kati ErdmannDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany. kati.erdmann@uniklinikum-dresden.de.ORCID http://orcid.org/0000-0003-3717-3637
Knut KaulkeDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Christiane RiegerDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Karsten SalomoDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Manfred P WirthDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Susanne FuesselDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Technische Universität Dresden · DEKlinik und Poliklinik für Psychotherapie und Psychosomatik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe tumor-suppressive microRNAs miR-26a and miR-138 are significantly down-regulated in prostate cancer (PCa) and have been identified as direct regulators of enhancer of zeste homolog 2 (EZH2), which is a known oncogene in PCa. In the present study, the influence of miR-26a and miR-138 on EZH2 and cellular function including the impact on the cell cycle regulating network was evaluated in PCa cells.

methodsPC-3 and DU-145 PCa cells were transfected with 100 nM of miRNA mimics, siRNA against EZH2 (siR-EZH2) or control constructs for 4 h. Analyses of gene expression and cellular function were conducted 48 h after transfection.

resultsBoth miRNAs influenced the EZH2 expression and activity only marginally, whereas siR-EZH2 led to a notable decrease of the EZH2 expression and activity. Both miRNAs inhibited short- and/or long-term proliferation of PCa cells but showed no effect on viability and apoptosis. In PC-3 cells, miR-26a and miR-138 caused a significant surplus of cells in the G0/G1 phase of 6 and 12 %, respectively, thus blocking the G1/S-phase transition. Treatment with siR-EZH2 was without substantial influence on cellular function and cell cycle. Therefore, alternative target genes involved in cell cycle regulation were identified in silico. MiR-26a significantly diminished the expression of its targets CCNE1, CCNE2 and CDK6, whereas CCND1, CCND3 and CDK6 were suppressed by their regulator miR-138.

conclusionsThe present findings suggest an anti-proliferative role for miR-26a and miR-138 in PCa by blocking the G1/S-phase transition independent of EZH2 but via a concerted inhibition of crucial cell cycle regulators.

Indexed as

Biomimetic MaterialsCell Line, TumorEnhancer of Zeste Homolog 2 ProteinG1 Phase Cell Cycle CheckpointsHumansMaleMicroRNAsProstatic NeoplasmsRNA, Small InterferingS PhaseTransfectionEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMicroRNAsMIRN138 microRNA, humanMIRN26 microRNA, humanRNA, Small InterferingCell cycleEnhancer of zeste homolog 2 (EZH2)MicroRNAsMiR-138MiR-26aProstate cancer

Identifiers

PMID27562865
PMCPMC11818972
OpenAlexW2511684183

What OpenQuestion holds

Textmetadata
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.