Evidence map›Paper›PMID 31409902›Full record

ArticleOncogene2019

DLC1 deficiency and YAP signaling drive endothelial cell contact inhibition of growth and tumorigenesis.

Lisa Ritchey, Taekyu Ha, Atsushi Otsuka, Kenji Kabashima, Dunrui Wang, Yuyi Wang, Douglas R Lowy, Giovanna Tosato

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2019. 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
1.0field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Genes & diseases · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. 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

8 authors at 4 institutions in 2 countries.

Lisa Ritchey *Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Taekyu Ha *Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Atsushi OtsukaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kenji KabashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Dunrui WangLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Yuyi WangLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Douglas R LowyLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Giovanna TosatoLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. tosatog@mail.nih.gov.
National Institutes of Health · USKyoto University · JPCenter for Cancer Research · USNational Cancer Institute · US

Funding

Angiogenesis and Tumor GrowthZIASC010355 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI TOSATO, GIOVANNA · 2009 to 2025
$13.3M
Intramural NIH HHS ZIA SC010355
6 · The paper itself

Abstract

Deleted in Liver Cancer 1 (DLC1) is a tumor suppressor gene deleted in many cancers, including angiosarcoma, an aggressive malignancy of endothelial cell derivation. DLC1-deficiency in primary endothelial cells causes the loss of cell contact inhibition of growth through incompletely defined mechanisms. We report that DLC1 is a regulator of YAP, a transcriptional coactivator of proliferation-promoting and tumor-promoting genes; when confluent, active/nuclear YAP was significantly more abundant in DLC1-deficient endothelial cells compared with control cells. We also found that YAP is a required effector of the loss of cell contact inhibition of growth manifested by DLC1-deficient endothelial cells, as the silencing of YAP prevents this loss. Consistently, human angiosarcomas specimens contained a significantly greater proportion of DLC1

Indexed as

Contact InhibitionAdaptor Proteins, Signal TransducingAnimalsCell MovementCell ProliferationCell Transformation, NeoplasticEndothelial CellsFemaleGTPase-Activating ProteinsHemangiosarcomaHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred BALB CSignal TransductionTranscription FactorsAdaptor Proteins, Signal TransducingDLC1 protein, humanGTPase-Activating ProteinsTranscription FactorsTumor Suppressor ProteinsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID31409902
PMCPMC8276116
OpenAlexW2968761716

What OpenQuestion holds

Textmetadata
LicenceTDM
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.