Evidence map›Paper›PMID 28467797›Full record

ArticleOncotarget2017

Synergistic inhibition effect of TNIK inhibitor KY-05009 and receptor tyrosine kinase inhibitor dovitinib on IL-6-induced proliferation and Wnt signaling pathway in human multiple myeloma cells.

Yura Lee, Jung-Il Jung, Kyeong-Yong Park, Soon Ae Kim, Jiyeon Kim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. BRAT1 - a new therapeutic target for glioblastoma.Cellular and molecular life sciences : CMLS · 2025
    Article
  3. TNIK in disease: from molecular insights to therapeutic prospects.Apoptosis : an international journal on programmed cell death · 2024
    Review
  4. Article
  5. Article
  6. Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
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

5 authors at 2 institutions in 1 country.

Yura LeeDepartment of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 34824, Korea.
Jung-Il JungDepartment of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 34824, Korea.
Kyeong-Yong ParkR&D Center, Peptron, Inc., Daejeon 34054, Korea.
Soon Ae KimDepartment of Pharmacology, School of Medicine, Eulji University, Daejeon 34824, Korea.
Jiyeon KimDepartment of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 34824, Korea.
Eulji University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma is a fetal form of plasma cell malignancy characterized by abnormal clonal proliferation of plasma cells. Especially, the canonical Wnt signaling pathway mediated by β-catenin is activated in multiple myeloma cells, stimulating their proliferation. Here, we investigated the relationship between interleukin-6-induced proliferation of multiple myeloma cells and Traf2- and Nck-interacting kinase (TNIK) expression in Wnt signaling. Interleukin-6 increased the proliferation of multiple myeloma cells and TNIK mRNA and protein expression. In addition, we examined the effect on TNIK of TNIK inhibitor KY-05009 and receptor tyrosine kinase inhibitor dovitinib and whether inhibition of TNIK suppresses the interleukin-6-induced proliferation of multiple myeloma cells. KY-05009 and dovitinib synergistically inhibited interleukin-6-stimulated proliferation and induced apoptosis through the inhibition of Wnt signaling in MM cells. Our results provide crucial information that TNIK is involved in the interleukin-6-dependent proliferation of multiple myeloma cells and inhibition of Wnt signaling involving TNIK could be a therapeutic strategy for the treatment of interleukin-6-dependent multiple myeloma.

Indexed as

Aniline CompoundsApoptosisBenzimidazolesbeta CateninCell Line, TumorCell ProliferationCell SurvivalDrug SynergismGene Expression Regulation, NeoplasticGerminal Center KinasesHumansInterleukin-6Multiple MyelomaProtein Kinase InhibitorsProtein Serine-Threonine KinasesQuinolones4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one5-(4-methylbenzamido)-2-(phenylamino)thiazole-4-carboxamideAniline CompoundsBenzimidazolesbeta CateninGerminal Center KinasesInterleukin-6Protein Kinase InhibitorsProtein Serine-Threonine KinasesQuinolonesThiazolesTNIK protein, humanIL-6KY-05009multiple myelomaTNIKWnt signaling

Identifiers

PMID28467797
PMCPMC5522218
OpenAlexW2606989726

What OpenQuestion holds

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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.