Evidence map›Paper›PMID 31285446›Full record

ArticleScientific reports2019

mTOR Signaling Upregulates CDC6 via Suppressing miR-3178 and Promotes the Loading of DNA Replication Helicase.

Xianjin Wu, Shenghua Li, Xing Hu, Xiaoliang Xiang, Megan Halloran, Linlin Yang, Terence M Williams, Peter J Houghton, Changxian Shen, Zhengfu He

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Polyploidy and mTOR signaling: a possible molecular link.Cell communication and signaling : CCS · 2024
    Review
  3. Article
  4. Article
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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 2 countries.

Xianjin WuKey Laboratory of Hunan Province for Study and Utilization of Ethnic Medicinal Plant Resources, College of Biological and Food Engineering, Huaihua University, Huaihua, 418008, China.
Shenghua LiKey Laboratory of Hunan Province for Study and Utilization of Ethnic Medicinal Plant Resources, College of Biological and Food Engineering, Huaihua University, Huaihua, 418008, China.
Xing HuKey Laboratory of Hunan Province for Study and Utilization of Ethnic Medicinal Plant Resources, College of Biological and Food Engineering, Huaihua University, Huaihua, 418008, China.
Xiaoliang XiangKey Laboratory of Hunan Province for Study and Utilization of Ethnic Medicinal Plant Resources, College of Biological and Food Engineering, Huaihua University, Huaihua, 418008, China.
Megan HalloranComprehensive Cancer Center, The Ohio State University, Columbus, Ohio, 43210, USA.
Linlin YangComprehensive Cancer Center, The Ohio State University, Columbus, Ohio, 43210, USA.
Terence M WilliamsComprehensive Cancer Center, The Ohio State University, Columbus, Ohio, 43210, USA.
Peter J HoughtonThe Greehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, 78229, USA.
Changxian ShenComprehensive Cancer Center, The Ohio State University, Columbus, Ohio, 43210, USA. shen.637@osu.edu.ORCID http://orcid.org/0000-0002-7668-7166
Zhengfu HeDepartment of Thoracic Surgery, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, 310016, China. hezhengfu123@hotmail.com.
Huaihua University · CNThe Ohio State University · USSir Run Run Shaw Hospital · CNThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

mTOR signaling pathway is deregulated in most cancers and uncontrolled cell cycle progression is a hallmark of cancer cell. However, the precise molecular mechanisms of the regulation of DNA replication and chromatin metabolism by mTOR signaling are largely unknown. We herein report that mTOR signaling promotes the loading of MCM2-7 helicase onto chromatin and upregulates DNA replication licensing factor CDC6. Pharmacological inhibition of mTOR kinase resulted in CHK1 checkpoint activation and decreased MCM2-7 replication helicase and PCNA associated with chromatins. Further pharmacological and genetic studies demonstrated CDC6 is positively controlled by mTORC1-S6K1 and mTORC2 signaling. miRNA screening revealed mTOR signaling suppresses miR-3178 thereby upregulating CDC6. Analysis of TCGA data found that CDC6 is overexpressed in most cancers and associates with the poor survival of cancer patients. Our findings suggest that mTOR signaling may control DNA replication origin licensing and replisome stability thereby cell cycle progression through CDC6 regulation.

Indexed as

Signal TransductionCell Cycle ProteinsCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHeLa CellsHumansMicroRNAsMinichromosome Maintenance ProteinsNuclear ProteinsProliferating Cell Nuclear AntigenRhabdomyosarcomaTOR Serine-Threonine KinasesUp-RegulationCDC6 protein, humanCell Cycle ProteinsMicroRNAsMinichromosome Maintenance ProteinsMIRN3178 microRNA, humanMTOR protein, humanNuclear ProteinsPCNA protein, humanProliferating Cell Nuclear AntigenTOR Serine-Threonine Kinases

Identifiers

PMID31285446
PMCPMC6614418
OpenAlexW2960943556

What OpenQuestion holds

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LicenceCC BY
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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.