Evidence map›Paper›PMID 22945237›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2013

The maternal embryonic leucine zipper kinase (MELK) is upregulated in high-grade prostate cancer.

Ruprecht Kuner, Maria Fälth, Nicole Chui Pressinotti, Jan C Brase, Sabrina Balaguer Puig, Jennifer Metzger, Stephan Gade, Georg Schäfer, Georg Bartsch, Eberhard Steiner and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 3 pooled it
3.0field-weighted citation impact, top 9% 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

104 citing papers in PubMed, 3 syntheses or guidelines pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Chromatin regulatorsChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026
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  16. Targeting MELK in tumor cells and tumor microenvironment: from function and mechanism to therapeutic application.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  17. Article
  18. Article
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  20. Review

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

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

12 authors at 2 institutions in 2 countries.

Ruprecht KunerUnit Cancer Genome Research, Division of Molecular Genetics, German Cancer Research Center and National Center of Tumor Diseases, Im Neuenheimer Feld 460, 69120, Heidelberg, Germany. r.kuner@dkfz.de
Maria Fälth
Nicole Chui Pressinotti
Jan C Brase
Sabrina Balaguer Puig
Jennifer Metzger
Stephan Gade
Georg Schäfer
Georg Bartsch
Eberhard Steiner
Helmut Klocker
Holger Sültmann
German Cancer Research Center · DEInnsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of cell cycle control is a prerequisite for cancer onset and progression. In prostate cancer, increased activity of cell cycle genes has been associated with prognostic parameters such as biochemical relapse and survival. The identification of novel oncogenic and druggable targets in patient subgroups with poor prognosis may help to develop targeted therapy approaches. We analyzed prostate cancer and corresponding benign tissues (n = 98) using microarrays. The comparison of high- and low-grade tumors (Gleason score ≥ 4 + 3 vs. ≤ 3 + 4) revealed 144 differentially expressed genes (p < 0.05). Out of these, 15 genes were involved in the cell cycle process. The gene maternal embryonic leucine zipper kinase (MELK) was identified to be highly correlated with cell cycle genes like UBE2C, TOP2A, CCNB2, and AURKB. Increased MELK gene expression in high-risk prostate cancer was validated by qPCR in an independent patient cohort (p < 0.005, n = 79). Immunohistochemistry analysis using a tissue microarray (n = 94) revealed increased MELK protein expression in prostate cancer tissues of high Gleason scores. RNAi-based inhibition of MELK in PC3 and LNCaP cells suggested putative function in chromatin modification, embryonic development and cell migration. The concerted inhibition of MELK and other cell cycle targets by the antibiotic siomycin A strongly impaired cell viability of prostate cancer cells, and may point to a novel therapy approach for a subset of high-risk prostate cancer patients.

Indexed as

Gene Expression Regulation, NeoplasticAgedAnti-Bacterial AgentsCell Line, TumorCell SurvivalHumansMaleMiddle AgedPeptidesPrognosisProstatic NeoplasmsProtein Serine-Threonine KinasesRNA InterferenceUp-RegulationAnti-Bacterial AgentsMELK protein, humanPeptidesProtein Serine-Threonine Kinasessiomycin A

Identifiers

PMID22945237
OpenAlexW1996612168

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.