Evidence map›Paper›PMID 30392041›Full record

ArticleCellular and molecular life sciences : CMLS2019

Induction of apoptosis in ovarian cancer cells by miR-493-3p directly targeting AKT2, STK38L, HMGA2, ETS1 and E2F5.

Michael Kleemann, Helga Schneider, Kristian Unger, Jeremias Bereuther, Simon Fischer, Philip Sander, E Marion Schneider, Pamela Fischer-Posovszky, Christian U Riedel, René Handrick and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2019. 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
1.6field-weighted citation impact, top 18% 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, 42 citations in OpenAlex.

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  13. Mediator subunit MED1 is required for E2A-PBX1-mediated oncogenic transcription and leukemic cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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.

Michael KleemannInstitute of Applied Biotechnology, University of Applied Sciences Biberach, Hubertus-Liebrecht-Str. 35, 88400, Biberach, Germany. kleemann@hochschule-bc.de.ORCID http://orcid.org/0000-0002-1924-5249
Helga SchneiderInstitute of Applied Biotechnology, University of Applied Sciences Biberach, Hubertus-Liebrecht-Str. 35, 88400, Biberach, Germany.
Kristian UngerResearch Unit Radiation Cytogenetics, Helmholtz Zentrum München Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764, Neuherberg, Germany.
Jeremias BereutherApceth Biopharma GmbH, Haidgraben 5, 85521, Ottobrunn, Germany.
Simon FischerBoehringer Ingelheim Pharma GmbH & Co. KG, Bioprocess and Analytical Development, Birkendorfer Straße 65, 88400, Biberach, Germany.
Philip SanderDivision of Experimental Anesthesiology, University Medical Center Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
E Marion SchneiderDivision of Experimental Anesthesiology, University Medical Center Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Pamela Fischer-PosovszkyDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Eythstr. 24, 89075, Ulm, Germany.
Christian U RiedelFaculty of Medicine, University of Ulm, Albert-Einstein-Alee 11, 89081, Ulm, Germany.
René HandrickInstitute of Applied Biotechnology, University of Applied Sciences Biberach, Hubertus-Liebrecht-Str. 35, 88400, Biberach, Germany.
Kerstin OtteInstitute of Applied Biotechnology, University of Applied Sciences Biberach, Hubertus-Liebrecht-Str. 35, 88400, Biberach, Germany.
Universität Ulm · DEUniversity of Applied Sciences Biberach · DEApceth Biopharma (Germany) · DEBoehringer Ingelheim (Germany) · DEHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis is a form of directed programmed cell death with a tightly regulated signalling cascade for the destruction of single cells. MicroRNAs (miRNAs) play an important role as fine tuners in the regulation of apoptotic processes. MiR-493-3p mimic transfection leads to the induction of apoptosis causing the breakdown of mitochondrial membrane potential and the activation of Caspases resulting in the fragmentation of DNA in several ovarian carcinoma cell lines. Ovarian cancer shows with its pronounced heterogeneity a very high death-to-incidence ratio. A target gene analysis for miR-493-3p was performed for the investigation of underlying molecular mechanisms involved in apoptosis signalling pathways. Elevated miR-493-3p levels downregulated the mRNA and protein expression levels of Serine/Threonine Kinase 38 Like (STK38L), High Mobility Group AT-Hook 2 (HMGA2) and AKT Serine/Threonine Kinase 2 (AKT2) by direct binding as demonstrated by luciferase reporter assays. Notably, the protein expression of RAF1 Proto-Oncogene, Serine/Threonine Kinase (RAF1) was almost completely downregulated by miR-493-3p. This interaction, however, was indirect and regulated by STK38L phosphorylation. In addition, RAF1 transcription was diminished as a result of reduced transcription of ETS proto-oncogene 1 (ETS1), another direct target of miR-493-3p. Taken together, our observations have uncovered the apoptosis inducing potential of miR-493-3p through its regulation of multiple target genes participating in the extrinsic and intrinsic apoptosis pathway.

Indexed as

Drug Delivery SystemsApoptosisBinding SitesE2F5 Transcription FactorFemaleGene Expression Regulation, NeoplasticHMGA2 ProteinHumansMicroRNAsOvarian NeoplasmsProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-aktSignal TransductionAKT2 protein, humanE2F5 protein, humanE2F5 Transcription FactorETS1 protein, humanHMGA2 ProteinHMGA2 protein, humanMAS1 protein, humanMicroRNAsMIRN493 microRNA, humanProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-aktSTK38L protein, humanCancerMicroRNARAF1Signalling pathwaysTargets

Identifiers

PMID30392041
PMCPMC11105321
OpenAlexW2898785698

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.