Evidence map›Paper›PMID 24553121›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells.

Yuko Murakami-Tonami, Satoshi Kishida, Ichiro Takeuchi, Yuki Katou, John M Maris, Hitoshi Ichikawa, Yutaka Kondo, Yoshitaka Sekido, Katsuhiko Shirahige, Hiroshi Murakami and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 7 institutions in 2 countries.

Yuko Murakami-TonamiDepartment of Molecular Biology; Nagoya University Graduate School of Medicine; Nagoya, Japan.
Satoshi KishidaDepartment of Molecular Biology; Nagoya University Graduate School of Medicine; Nagoya, Japan.
Ichiro TakeuchiDepartment of Computer Science/Scientific and Engineering Simulation; Nagoya Institute of Technology; Nagoya, Japan.
Yuki KatouLaboratory of Genome Structure & Function; Institute of Molecular and Cellular Biosciences; The University of Tokyo; Tokyo, Japan.
John M MarisDepartment of Pediatrics and Center for Childhood Cancer Research; Children's Hospital of Philadelphia; University of Pennsylvania; Philadelphia, PA USA.
Hitoshi IchikawaDivision of Genetics; National Cancer Institute; Tokyo, Japan.
Yutaka KondoDivision of Molecular Oncology; Aichi Cancer Center Research Institute; Nagoya, Japan; Division of Epigenomics; Aichi Cancer Center Research Institute; Nagoya, Japan.
Yoshitaka SekidoDivision of Molecular Oncology; Aichi Cancer Center Research Institute; Nagoya, Japan.
Katsuhiko ShirahigeLaboratory of Genome Structure & Function; Institute of Molecular and Cellular Biosciences; The University of Tokyo; Tokyo, Japan.
Hiroshi MurakamiDepartment of Biological Science; Faculty of Science and Engineering; Chuo University; Tokyo, Japan.
Kenji KadomatsuDepartment of Molecular Biology; Nagoya University Graduate School of Medicine; Nagoya, Japan.
Nagoya University · JPMolecular Oncology (United States) · USChildren's Hospital of Philadelphia · USChuo University · JPDivision of Molecular & Cellular Biosciences · USNagoya Institute of Technology · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The condensin complex is required for chromosome condensation during mitosis; however, the role of this complex during interphase is unclear. Neuroblastoma is the most common extracranial solid tumor of childhood, and it is often lethal. In human neuroblastoma, MYCN gene amplification is correlated with poor prognosis. This study demonstrates that the gene encoding the condensin complex subunit SMC2 is transcriptionally regulated by MYCN. SMC2 also transcriptionally regulates DNA damage response genes in cooperation with MYCN. Downregulation of SMC2 induced DNA damage and showed a synergistic lethal response in MYCN-amplified/overexpression cells, leading to apoptosis in human neuroblastoma cells. Finally, this study found that patients bearing MYCN-amplified tumors showed improved survival when SMC2 expression was low. These results identify novel functions of SMC2 in DNA damage response, and we propose that SMC2 (or the condensin complex) is a novel molecular target for the treatment of MYCN-amplified neuroblastoma.

Indexed as

Adenosine TriphosphatasesAnimalsApoptosisCarrier ProteinsCell Cycle ProteinsCell Line, TumorChromosomal Proteins, Non-HistoneDNA DamageGenome-Wide Association StudyHEK293 CellsHumansMiceNeuroblastomaN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsAdenosine TriphosphatasesCarrier ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneMYCN protein, humanMYCN protein, mouseN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsProto-Oncogene ProteinsSMC2 protein, humanSMC2 protein, mouseSMC4 protein, humancondensin complexDNA damage responseMYCNneuroblastomasynergistic lethal response

Identifiers

PMID24553121
PMCPMC4013162
OpenAlexW2041539092

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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.