Evidence map›Paper›PMID 23874387›Full record

ArticlePloS one2013

Transcriptional repression of Bim by a novel YY1-RelA complex is essential for the survival and growth of Multiple Myeloma.

Veena Potluri, Sunil K Noothi, Subrahmanya D Vallabhapurapu, Sang-Oh Yoon, James J Driscoll, Charles H Lawrie, Sivakumar Vallabhapurapu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  8. The DNA-helicase HELLS drives ALKCell death & disease · 2021
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  19. Gene set enrichment analysis of the NF-κB/Snail/YY1/RKIP circuitry in multiple myeloma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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 2 institutions in 3 countries.

Veena PotluriDepartment of Cancer and Cell Biology, College of Medicine, University of Cincinnati, Cincinnati, Ohio, United States of America.
Sunil K Noothi
Subrahmanya D Vallabhapurapu
Sang-Oh Yoon
James J Driscoll
Charles H Lawrie
Sivakumar Vallabhapurapu
University of Cincinnati · USUniversity of Oxford · GB

Funding

Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E. · 2012 to 2014
$9.9M
NCATS NIH HHS UL1 TR000077
6 · The paper itself

Abstract

Multiple Myeloma (MM) is an incurable plasma cell cancer that is caused by several chromosomal translocations and gene deletions. Although deregulation of several signaling pathways including the Nuclear Factor-Kappa B (NF-κB) pathway has been reported in MM, the molecular requirement and the crosstalk between NF-κB and its target genes in MM cell survival has been largely unclear. Here, we report that Yin Yang1 (YY1), a target gene for NF-κB, is hyperexpressed in most MM tumor cells obtained from human patients, exhibits constitutive nuclear localization, and is essential for survival of MM cells. Mechanistically, we report a novel YY1-RelA complex formation, which is essential to transcriptionally repress a proapoptotic gene Bim. In line with this, depletion of YY1 or RelA resulted in elevated levels of Bim and apoptosis. Moreover, both YY1 and RelA are recruited to the Bim promoter and are required to repress the Bim promoter. Importantly, depletion of YY1 or RelA almost completely impaired the colony forming ability of MM progenitor cells suggesting that both RelA and YY1 are essential for the survival and growth of MM progenitor cells. Moreover, depletion of either YY1 or RelA completely inhibited MM tumor growth in xenograft models for human myeloma. Thus, a novel RelA-YY1 transcriptional repression complex is an attractive drug target in MM.

Indexed as

Cell ProliferationRNA InterferenceAnimalsApoptosis Regulatory ProteinsBcl-2-Like Protein 11Cell SurvivalHEK293 CellsHumansMembrane ProteinsMiceMice, NudeMultiple MyelomaMultiprotein ComplexesProto-Oncogene ProteinsRNA, Small InterferingTranscription Factor RelAApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11Membrane ProteinsMultiprotein ComplexesProto-Oncogene ProteinsRELA protein, humanRNA, Small InterferingTranscription Factor RelAYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID23874387
PMCPMC3707888
OpenAlexW2046459638

What OpenQuestion holds

Textmetadata
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.