Evidence map›Paper›PMID 28114277›Full record

ArticleOncogene2017

The novel MKL target gene myoferlin modulates expansion and senescence of hepatocellular carcinoma.

C Hermanns, V Hampl, K Holzer, A Aigner, J Penkava, N Frank, D E Martin, K C Maier, N Waldburger, S Roessler and 7 more

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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
1.9field-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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  6. Article
  7. Otoferlin as a multirole CaFrontiers in cellular neuroscience · 2023
    Review
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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

17 authors at 6 institutions in 1 country.

C HermannsWalther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University Munich, Munich, Germany.
V HamplWalther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University Munich, Munich, Germany.
K HolzerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
A AignerRudolf Boehm Institute of Pharmacology and Toxicology, Clinical Pharmacology, University of Leipzig, Leipzig, Germany.
J PenkavaWalther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University Munich, Munich, Germany.
N FrankWalther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University Munich, Munich, Germany.
D E MartinGene Center, Department of Chemistry and Pharmacy, Ludwig-Maximilians-University Munich, Munich, Germany.
K C MaierGene Center, Department of Chemistry and Pharmacy, Ludwig-Maximilians-University Munich, Munich, Germany.
N WaldburgerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
S RoesslerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0002-5333-5942
M Goppelt-StruebeDepartment of Nephrology and Hypertension, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
I AkrapInterfaculty Institute of Cell Biology, Tuebingen University, Tuebingen, Germany.
A ThavamaniInterfaculty Institute of Cell Biology, Tuebingen University, Tuebingen, Germany.
S SingerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
A NordheimInterfaculty Institute of Cell Biology, Tuebingen University, Tuebingen, Germany.
T GudermannWalther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University Munich, Munich, Germany.
S MuehlichWalther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DEHeidelberg University · DEUniversity of Tübingen · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEGerman Cancer Research Center · DELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Megakaryoblastic Leukemia 1 and 2 (MKL1/2) are transcriptional coactivators of Serum Response Factor (SRF) with an essential role for hepatocellular carcinoma (HCC) growth and oncogene-induced senescence. In this report, we identified myoferlin as a novel MKL/SRF target gene by gene expression profiling and verification in vivo in HCC xenografts. Myoferlin was overexpressed in human and murine HCCs triggered by conditional expression of constitutively active SRF-VP16 protein in hepatocytes. Furthermore, myoferlin was required for HCC cell invasion, proliferation and anchorage-independent cell growth. We provide evidence that myoferlin is a crucial gene target of MKL1/2 mediating its effect on oncogene-induced senescence by modulating the activation state of the EGFR and downstream MAPK and p16-/Rb pathways. Depletion of myoferlin in tumour cells from SRF-VP16-derived murine HCCs induced a senescence phenotype. These findings identify MKL1/2 and myoferlin as novel therapeutic targets to treat human HCC by a senescence-inducing strategy.

Indexed as

AnimalsCalcium-Binding ProteinsCarcinoma, HepatocellularCell Line, TumorCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMembrane ProteinsMiceMuscle ProteinsNeoplasm InvasivenessNeoplasm TransplantationNIH 3T3 CellsSerum Response FactorCalcium-Binding ProteinsMembrane ProteinsMRTFA protein, humanMRTFB protein, humanMuscle ProteinsMYOF protein, humanSerum Response FactorSRF protein, humanTrans-ActivatorsTranscription Factors

Identifiers

PMID28114277
OpenAlexW2581071658

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.