Evidence map›Paper›PMID 24286317›Full record

ArticleBMB reports2014

Down-modulation of Bis reduces the invasive ability of glioma cells induced by TPA, through NF-κB mediated activation of MMP-9.

Young Dae Lee, Mei Nu Cui, Hye Hyeon Yoon, Hye Yun Kim, Il-Hoan Oh, Jeong-Hwa Lee

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
10.5field-weighted citation impact, top 3% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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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 2 institutions in 2 countries.

Young Dae LeeDepartment of Biochemistry, Cancer Research Institute, Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
Mei Nu CuiDepartment of Biochemistry, Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
Hye Hyeon YoonDepartment of Biochemistry, Cancer Research Institute, Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
Hye Yun KimDepartment of Biochemistry, Cancer Research Institute, Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
Il-Hoan OhCancer Evolution Research Center, Catholic High-Performance Cell Therapy Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
Jeong-Hwa LeeDepartment of Biochemistry, Cancer Research Institute, Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
Cancer Research Institute · USCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bcl-2 interacting cell death suppressor (Bis) has been shown to have anti-apoptotic and anti-stress functions. Recently, increased Bis expression was reported to correlate with glioma aggressiveness. Here, we investigated the effect of Bis knockdown on the acquisition of the invasive phenotype of A172 glioma cells, induced by 12-O-Tetradecanoylphorbol-3-acetate (TPA), using a Transwell assay. Bis knockdown resulted in a significant decrease in the migration and invasion of A172 cells. Furthermore, Bis knockdown notably decreased TPA-induced matrix metalloproteinase-9 (MMP-9) activity and mRNA expression, as measured by zymography and quantitative real time PCR, respectively. A luciferase reporter assay indicated that Bis suppression significantly down-regulated NF-κB-driven transcription. Finally, we demonstrated that the rapid phosphorylation and subsequent degradation of IκB-α induced by TPA was remarkably delayed by Bis knockdown. These results suggest that Bis regulates the invasive ability of glioma cells elicited by TPA, by modulating NF-κB activation, and subsequent induction of MMP-9 mRNA.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCell Line, TumorCell MovementDown-RegulationEnzyme ActivationGene Knockdown TechniquesGliomaHumansI-kappa B ProteinsMatrix Metalloproteinase 9Neoplasm InvasivenessNF-KappaB Inhibitor alphaPhosphorylationRNA, MessengerRNA, NeoplasmAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBAG3 protein, humanI-kappa B ProteinsMatrix Metalloproteinase 9MMP9 protein, humanNF-KappaB Inhibitor alphaNFKBIA protein, humanRELA protein, humanRNA, MessengerRNA, NeoplasmTetradecanoylphorbol AcetateTranscription Factor RelA

Identifiers

PMID24286317
PMCPMC4163862
OpenAlexW2007114899

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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.