Evidence map›Paper›PMID 29022903›Full record

ReviewCell death & disease2017

Alternative mechanisms of miR-34a regulation in cancer.

Eva Slabáková, Zoran Culig, Ján Remšík, Karel Souček

Erratum issuedOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 160 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 3 pooled it
9.3field-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

160 citing papers in PubMed, 3 syntheses or guidelines pooled it, 263 citations in OpenAlex.

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100 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 2 countries.

Eva SlabákováDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czech Republic.
Zoran CuligCenter of Biomolecular and Cellular Engineering, International Clinical Research Center, St. Anne's University Hospital Brno, Brno, Czech Republic.
Ján RemšíkDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czech Republic.
Karel SoučekDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czech Republic.
Czech Academy of Sciences, Institute of Biophysics · CZInnsbruck Medical University · ATSt. Anne's University Hospital Brno · CZUniversity Hospital Brno · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA miR-34a is recognized as a master regulator of tumor suppression. The strategy of miR-34a replacement has been investigated in clinical trials as the first attempt of miRNA application in cancer treatment. However, emerging outcomes promote the re-evaluation of existing knowledge and urge the need for better understanding the complex biological role of miR-34a. The targets of miR-34a encompass numerous regulators of cancer cell proliferation, survival and resistance to therapy. MiR-34a expression is transcriptionally controlled by p53, a crucial tumor suppressor pathway, often disrupted in cancer. Moreover, miR-34a abundance is fine-tuned by context-dependent feedback loops. The function and effects of exogenously delivered or re-expressed miR-34a on the background of defective p53 therefore remain prominent issues in miR-34a based therapy. In this work, we review p53-independent mechanisms regulating the expression of miR-34a. Aside from molecules directly interacting with MIR34A promoter, processes affecting epigenetic regulation and miRNA maturation are discussed. Multiple mechanisms operate in the context of cancer-associated phenomena, such as aberrant oncogene signaling, EMT or inflammation. Since p53-dependent tumor-suppressive mechanisms are disturbed in a substantial proportion of malignancies, we summarize the effects of miR-34a modulation in cell and animal models in the clinically relevant context of disrupted or insufficient p53 function.

Indexed as

Genes, Tumor SuppressorAnimalsEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMicroRNAsNeoplasmsPromoter Regions, GeneticTumor Suppressor Protein p53MicroRNAsMIRN34 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID29022903
PMCPMC5682661
OpenAlexW2763422050

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.