Evidence map›Paper›PMID 28212583›Full record

ArticleOncotarget2017

Role of TOPK in lipopolysaccharide-induced breast cancer cell migration and invasion.

Min-Ah Seol, Jung-Hwan Park, Ji Heun Jeong, Jungmook Lyu, Seung Yun Han, Sang-Muk Oh

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  7. FYN/TOPK/HSPB1 axis facilitates the proliferation and metastasis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023
    Article
  8. Discovery of novel paeonol-based derivatives against skin inflammationJournal of enzyme inhibition and medicinal chemistry · 2022
    Article
  9. Article
  10. Global DNA Methylation Profiles in Peripheral Blood of WTC-Exposed Community Members with Breast Cancer.International journal of environmental research and public health · 2022
    Article
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  12. Review
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  15. 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

6 authors at 1 institution in 1 country.

Min-Ah SeolDepartment of Biochemistry, College of Medicine, Konyang University, Daejeon, Korea.
Jung-Hwan ParkDepartment of Biochemistry, College of Medicine, Konyang University, Daejeon, Korea.
Ji Heun JeongDepartment of Anatomy, College of Medicine, Konyang University, Daejeon, Korea.
Jungmook LyuDepartment of Medical Science, Konyang University, Daejeon, Korea.
Seung Yun HanDepartment of Anatomy, College of Medicine, Konyang University, Daejeon, Korea.
Sang-Muk OhDepartment of Biochemistry, College of Medicine, Konyang University, Daejeon, Korea.
Konyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation has been known to be linked to invasion or metastasis of breast cancer, which has poor prognosis, although the regulatory mechanism remains to be undiscovered. Here we show that T-LAK cell-originated protein kinase (TOPK) mediates pro-inflammatory endotoxin lipopolysaccharide (LPS)-induced breast cancer cell migration and invasion. The mRNA or protein level of TOPK, toll- like receptor4 (TLR4), interleukin (IL)-6, vascular endothelial growth factor (VEGF) or matrix metalloproteinase9 (MMP9) genes related to TLR4 signaling or tumor progression was induced by LPS treatment in MCF7 breast cancer cells, but the induction was abolished by stable knocking down of TOPK in MCF7 cells. Also, TOPK depletion decreased LPS-induced phosphorylation of p38, but not ERK and JNK among mitogen-activated protein kinases (MAPKs). On the other hand, we revealed that TOPK is essential for transcriptional activity of NF-κB or MMP9 promoter triggered by LPS. The induced promoter activity of NF-κB or MMP9 but not AP-1 was inhibited by knocking down of TOPK. Furthermore, we demonstrated that inhibitor of TOPK or MMP9 as well as MMP9 siRNA efficiently blocked LPS-induced migration or invasion of breast cancer cell lines. Interestingly, both of expression of TOPK and TLR4 were markedly increased in high-grade breast cancer. Collectively, we conclude that TOPK functions as a key mediator of LPS/TLR4-induced breast cancer cell migration and invasion through regulation of MMP9 expression or activity, implying a potential role of TOPK as a therapeutic target linking LPS-induced inflammation to breast cancer development.

Indexed as

Gene Expression Regulation, NeoplasticAdultAged, 80 and overBreast NeoplasmsCell Line, TumorCell MovementFemaleHumansLipopolysaccharidesMCF-7 CellsMiddle AgedMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesNeoplasm InvasivenessPhosphorylationToll-Like Receptor 4LipopolysaccharidesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPDZ-binding kinaseToll-Like Receptor 4breast cancerinvasionmatrix metalloproteinaseTOPK

Identifiers

PMID28212583
PMCPMC5522254
OpenAlexW2591567125

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.