Evidence map›Paper›PMID 29930325›Full record

ArticleNature communications2018

Mitotic polarization of transcription factors during asymmetric division establishes fate of forming cancer cells.

Yongqing Liu, Laura Siles, Xiaoqin Lu, Kevin C Dean, Miriam Cuatrecasas, Antonio Postigo, Douglas C Dean

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Asymmetric Cell Division and Tumor Heterogeneity.Frontiers in cell and developmental biology · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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 2 countries.

Yongqing LiuMolecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center, Louisville, KY, 40202, USA.
Laura SilesGroup of Transcriptional Regulation of Gene Expression, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), CIBERehd, 08010, Barcelona, Spain.
Xiaoqin LuDepartment of Ophthalmology and Visual Sciences, University of Louisville Health Sciences Center, Louisville, KY, 40202, USA.
Kevin C DeanDepartment of Ophthalmology and Visual Sciences, University of Louisville Health Sciences Center, Louisville, KY, 40202, USA.
Miriam CuatrecasasDepartment of Pathology, Centro de Diagnóstico Biomédico (CDB) Hospital Clínic, University of Barcelona, 08010, Barcelona, Spain.
Antonio PostigoMolecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center, Louisville, KY, 40202, USA. idib412@clinic.cat.
Douglas C DeanMolecular Targets Program, James Brown Cancer Center, University of Louisville Health Sciences Center, Louisville, KY, 40202, USA. dcdean01@louisville.edu.
University of Louisville · USConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ES

Funding

Molecular Determinants of Developmental DefectsP20GM103453 · NIGMS · UNIVERSITY OF LOUISVILLE · PI GREENE, ROBERT M · 2012 to 2012
$1.7M
Vision Research Infrastructure DevelopmentR24EY015636 · NEI · UNIVERSITY OF LOUISVILLE · PI KAPLAN, HENRY JERROLD · 2004 to 2008
$1.0M
NEI NIH HHS R24 EY015636NIGMS NIH HHS P20 GM103453
6 · The paper itself

Abstract

A model of K-Ras-initiated lung cancer was used to follow the transition of precancerous adenoma to adenocarcinoma. In hypoxic, Tgf-β1-rich interiors of adenomas, we show that adenoma cells divide asymmetrically to produce cancer-generating cells highlighted by epithelial mesenchymal transition and a CD44/Zeb1 loop. In these cells, Zeb1 represses the Smad inhibitor Zeb2/Sip1, causing Pten loss and launching Tgf-β1 signaling that drives nuclear translocation of Yap1. Surprisingly, the nuclear polarization of transcription factors during mitosis establishes parent and daughter fates prior to cytokinesis in sequential asymmetric divisions that generate cancer cells from precancerous lesions. Mutation or knockdown of Zeb1 in the lung blocked the production of CD44

Indexed as

Asymmetric Cell DivisionAdaptor Proteins, Signal TransducingAdenocarcinomaAdenomaAnimalsCell Cycle ProteinsCell PolarityEpithelial-Mesenchymal TransitionGene Knockdown TechniquesGenes, rasHumansHyaluronan ReceptorsLung NeoplasmsMiceMutationPhosphoproteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsHyaluronan ReceptorsPhosphoproteinsPTEN PhosphohydrolasePTEN protein, humanTranscription FactorsTransforming Growth Factor beta1Yap1 protein, mouseYAP-Signaling ProteinsZEB1 protein, mouseZEB2 protein, mouseZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2

Identifiers

PMID29930325
PMCPMC6013470
OpenAlexW2808491310

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.