Evidence map›Paper›PMID 25337588›Full record

ArticleJournal of cancer prevention2014

The Nuclear Matrix Protein, NRP/B, Acts as a Transcriptional Repressor of E2F-mediated Transcriptional Activity.

Jina Choi, Eun Sung Yang, Kiweon Cha, John Whang, Woo-Jung Choi, Shalom Avraham, Tae-Aug Kim

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cancer prevention, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024
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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

7 authors at 3 institutions in 2 countries.

Jina ChoiCHA Cancer Institute, CHA University, Seoul, Korea.
Eun Sung YangCancer Cell Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Kiweon ChaDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
John WhangCancer Cell Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Woo-Jung ChoiCHA Cancer Institute, CHA University, Seoul, Korea.
Shalom AvrahamDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Tae-Aug KimCHA Cancer Institute, CHA University, Seoul, Korea ; Cancer Cell Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
CHA University · KRBeth Israel Deaconess Medical Center · USHarvard University · US

Funding

HIV-1 gp120-mediated injury in brain endotheliumR01HL080699 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVRAHAM, SHALOM · 2004 to 2009
$1.7M
NHLBI NIH HHS R01 HL080699
6 · The paper itself

Abstract

backgroundNRP/B, a family member of the BTB/Kelch repeat proteins, is implicated in neuronal and cancer development, as well as the regulation of oxidative stress responses in breast and brain cancer. Our previous studies indicate that the NRP/B-BTB/POZ domain is involved in the dimerization of NRP/B and in a complex formation with the tumor suppressor, retinoblastoma protein. Although much evidence supports the potential role of NRP/B as a tumor suppressor, the molecular mechanisms of NRP/B action on E2F transcription factors have not been elucidated.

methodsThree-dimensional modeling of NRP/B was used to generate point mutations in the BTB/Kelch domains. Tet-on inducible NRP/B expression was established. The NRP/B deficient breast cancer cell line, MDA-MB-231, was generated using lentiviral shNRP/B to evaluate the effect of NRP/B on cell proliferation, invasion and migration. Immunoprecipitation was performed to verify the interaction of NRP/B with E2F and histone deacetylase (HDAC-1), and the expression level of NRP/B protein was analyzed by Western blot analysis. Changes in cell cycle were determined by flow cytometry. Transcriptional activities of E2F transcription factors were measured by chloramphenicol acetyltransferase (CAT) activity.

resultsEctopic overexpression of NRP/B demonstrated that the NRP/B-BTB/POZ domain plays a critical role in E2F-mediated transcriptional activity. Point mutations within the BTB/POZ domain restored E2-promoter activity inhibited by NRP/B. Loss of NRP/B enhanced the proliferation and migration of breast cancer cells. Endogenous NRP/B interacted with E2F and HDAC1. Treatement with an HDAC inhibitor, trichostatin A (TSA), abolished the NRP/B-mediated suppression of E2-promoter activity. Gain or loss of NRP/B in HeLa cells confirmed the transcriptional repressive capability of NRP/B on the E2F target genes, Cyclin E and HsORC (Homo sapiens Origin Recognition Complex).

conclusionsThe present study shows that NRP/B acts as a transcriptional repressor by interacting with the co-repressors, HDAC1, providing new insight into the molecular mechanisms of NRP/B on tumor suppression.

Indexed as

Breast cancerE2F transcription factorNRP/BTranscriptional activity

Identifiers

PMID25337588
PMCPMC4189505
OpenAlexW2071733507

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.