Evidence map›Paper›PMID 27494853›Full record

ArticleOncotarget2016

Met promotes the formation of double minute chromosomes induced by Sei-1 in NIH-3T3 murine fibroblasts.

Yantao Bao, Jia Liu, Jia You, Di Wu, Yang Yu, Chang Liu, Lei Wang, Fei Wang, Lu Xu, Liqun Wang and 15 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. FAPMolecular carcinogenesis · 2022
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. 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

25 authors.

Yantao BaoLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jia LiuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jia YouLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Di WuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Yang YuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Chang LiuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Lei WangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Fei WangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Lu XuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Liqun WangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Nan WangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Xing TianLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Falin WangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Hongbin LiangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Yating GaoLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Xiaobo CuiLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Guohua JiLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jing BaiLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jingcui YuScientific Research Centre, Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Xiangning MengLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Yan JinLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Wenjing SunLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Xin-Yuan GuanDepartment of Clinical Oncology, Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Chunyu ZhangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Songbin FuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSei-1 is an oncogene capable of inducing double minute chromosomes (DMs) formation. DMs are hallmarks of amplification and contribute to oncogenesis. However, the mechanism of Sei-1 inducing DMs formation remains unelucidated.

resultsDMs formation significantly increased during serial passage in vivo and gradually decreased following culture in vitro. micro nuclei (MN) was found to be responsible for the reduction. Of the DMs-carrying genes, Met was found to be markedly amplified, overexpressed and highly correlated with DMs formation. Inhibition of Met signaling decreased the number of DMs and reduced the amplification of the DMs-carrying genes. We identified a 3.57Mb DMs representing the majority population, which consists of the 1.21 Mb AMP1 from locus 6qA2 and the 2.36 Mb AMP2 from locus 6qA2-3. MATERIALS AND

methodsWe employed NIH-3T3 cell line with Sei-1 overexpression to monitor and characterize DMs in vivo and in vitro. Array comparative genome hybridization (aCGH) and fluorescence in situ hybridization (FISH) were performed to reveal amplification regions and DMs-carrying genes. Metaphase spread was prepared to count the DMs. Western blot and Met inhibition rescue experiments were performed to examine for involvement of altered Met signaling in Sei-1 induced DMs. Genomic walking and PCR were adopted to reveal DMs structure.

conclusionsMet is an important promotor of DMs formation.

Indexed as

Signal TransductionAnimalsBromodomain Containing ProteinsCell NucleusCell Transformation, NeoplasticChromosome AberrationsChromosomesComparative Genomic HybridizationGene AmplificationGenomeIn Situ Hybridization, FluorescenceMetaphaseMiceMice, Inbred BALB CMice, NudeMicronucleus TestsBromodomain Containing ProteinsMdm2 protein, mouseNuclear ProteinsProto-Oncogene Proteins c-mdm2Proto-Oncogene Proteins c-metSertad1 protein, mouseTrans-ActivatorsTranscription FactorsamplificationDMsin vivo passagemetSei-1

Identifiers

PMID27494853
PMCPMC5302943

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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.