Evidence map›Paper›PMID 31870133›Full record

ArticleMolecules and cells2020

The Tumor Suppressor, p53, Negatively Regulates Non-Canonical NF-κB Signaling through miRNAInduced Silencing of NF-κB-Inducing Kinase.

Hanbit Jang, Seulki Park, Jaehoon Kim, Jong Hwan Kim, Seon-Young Kim, Sayeon Cho, Sung Goo Park, Byoung Chul Park, Sunhong Kim, Jeong-Hoon Kim

Open access · greenAbstract read
In one paragraph

Article in Molecules and cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

12 citing papers in PubMed, 13 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

10 authors at 4 institutions in 1 country.

Hanbit JangDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Korea.
Seulki ParkDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
Jaehoon KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Korea.
Jong Hwan KimPersonalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea.
Seon-Young KimPersonalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea.
Sayeon ChoCollege of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Sung Goo ParkDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
Byoung Chul ParkDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
Sunhong KimDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
Jeong-Hoon KimDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
Korea Research Institute of Bioscience and Biotechnology · KRKorea University of Science and Technology · KRKorea Advanced Institute of Science and Technology · KRChung-Ang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NF-κB signaling through both canonical and non-canonical pathways plays a central role in immune responses and inflammation. NF-κB-inducing kinase (NIK) stabilization is a key step in activation of the non-canonical pathway and its dysregulation implicated in various hematologic malignancies. The tumor suppressor, p53, is an established cellular gatekeeper of proliferation. Abnormalities of the TP53 gene have been detected in more than half of all human cancers. While the non-canonical NF-κB and p53 pathways have been explored for several decades, no studies to date have documented potential cross-talk between these two cancer-related mechanisms. Here, we demonstrate that p53 negatively regulates NIK in an miRNA-dependent manner. Overexpression of p53 decreased the levels of NIK, leading to inhibition of the non-canonical NF-κB pathway. Conversely, its knockdown led to increased levels of NIK, IKKα phosphorylation, and p100 processing. Additionally, miR-34b induced by nutlin-3 directly targeted the coding sequences (CDS) of NIK. Treatment with anti-miR-34b-5p augmented NIK levels and subsequent non-canonical NF-κB signaling. Our collective findings support a novel cross-talk mechanism between non-canonical NF-κB and p53.

Indexed as

EndonucleasesGene Expression RegulationGene SilencingHeLa CellsHumansI-kappa B KinaseImidazolesMicroRNAsNF-kappa BPhosphorylationPiperazinesSignal TransductionTumor Suppressor Protein p53EndonucleasesI-kappa B KinaseImidazolesMicroRNAsMIRN34 microRNA, humanNF-kappa Bnutlin 3PiperazinesSND1 protein, humanTP53 protein, humanTumor Suppressor Protein p53cancermicroRNANF-κBNF-κB–inducing kinasep53tumor suppressor gene

Identifiers

PMID31870133
PMCPMC6999715
OpenAlexW3004751921

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.