Evidence map›Paper›PMID 26933922›Full record

ArticleOncotarget2016

Oncogenic roles of TOPK and MELK, and effective growth suppression by small molecular inhibitors in kidney cancer cells.

Taigo Kato, Hiroyuki Inoue, Seiya Imoto, Yoshinori Tamada, Takashi Miyamoto, Yo Matsuo, Yusuke Nakamura, Jae-Hyun Park

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. 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
  6. Review
  7. Targeting Apoptosis in Cancer.Current oncology reports · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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

8 authors at 3 institutions in 2 countries.

Taigo KatoDepartment of Medicine, The University of Chicago, Chicago, IL, USA.
Hiroyuki InoueDepartment of Medicine, The University of Chicago, Chicago, IL, USA.
Seiya ImotoHuman Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoshinori TamadaHuman Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Takashi MiyamotoOncoTherapy Science Inc., Kawasaki, Japan.
Yo MatsuoOncoTherapy Science Inc., Kawasaki, Japan.
Yusuke NakamuraDepartment of Medicine, The University of Chicago, Chicago, IL, USA.
Jae-Hyun ParkDepartment of Medicine, The University of Chicago, Chicago, IL, USA.
University of Chicago · USOncoTherapy Science (Japan) · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-lymphokine-activated killer cell-originated protein kinase (TOPK) and maternal embryonic leucine zipper kinase (MELK) have been reported to play critical roles in cancer cell proliferation and maintenance of stemness. In this study, we investigated possible roles of TOPK and MELK in kidney cancer cells and found their growth promotive effect as well as some feedback mechanism between these two molecules. Interestingly, the blockade of either of these two kinases effectively caused downregulation of forkhead box protein M1 (FOXM1) activity which is known as an oncogenic transcriptional factor in various types of cancer cells. Small molecular compound inhibitors against TOPK (OTS514) and MELK (OTS167) effectively suppressed the kidney cancer cell growth, and the combination of these two compounds additively worked and showed the very strong growth suppressive effect on kidney cancer cells. Collectively, our results suggest that both TOPK and MELK are promising molecular targets for kidney cancer treatment and that dual blockade of OTS514 and OTS167 may bring additive anti-tumor effects with low risk of side effects.

Indexed as

ApoptosisCarcinoma, Renal CellCell Line, TumorCell ProliferationDown-RegulationForkhead Box Protein M1Gene Knockdown TechniquesHumansKidney NeoplasmsMitogen-Activated Protein Kinase KinasesMolecular Targeted TherapyPhosphorylationProtein Kinase InhibitorsProtein Serine-Threonine KinasesSmall Molecule LibrariesTransfectionForkhead Box Protein M1FOXM1 protein, humanMELK protein, humanMitogen-Activated Protein Kinase KinasesPDZ-binding kinaseProtein Kinase InhibitorsProtein Serine-Threonine KinasesSmall Molecule Librarieskidney cancerkinase inhibitorMELKmolecular targetTOPK

Identifiers

PMID26933922
PMCPMC4951240
OpenAlexW2289208337

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.