Evidence map›Paper›PMID 28408355›Full record

ArticleCancer letters2017

Down-regulation of DLC1 in endothelial cells compromises the angiogenesis process.

Yi-Ping Shih, Sarah Y Yuan, Su Hao Lo

Abstract read
In one paragraph

Article in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Genes & diseases · 2026
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  8. Genes & diseases · 2022
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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

3 authors at 2 institutions in 1 country.

Yi-Ping ShihDepartment of Biochemistry and Molecular Medicine, California-Davis, Sacramento, CA 95817, USA.
Sarah Y YuanDepartment of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Su Hao LoDepartment of Biochemistry and Molecular Medicine, California-Davis, Sacramento, CA 95817, USA. Electronic address: shlo@ucdavis.edu.
University of California, Davis · USUniversity of South Florida · US

Funding

Microvascular Barrier Dysfunction in Thermal TraumaR01HL070752 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2002 to 2018
$4.7M
Training Program in Oncogenic Signals and Chromosome BiologyT32CA108459 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HEYER, WOLF-DIETRICH · 2006 to 2020
$3.6M
Mechanism of DLC1-mediated tumor suppressionR01CA151366 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LO, SU HAO · 2010 to 2014
$1.5M
Neutrophil Activation and Microvascular HyperpermeabilityR01HL126646 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2016 to 2019
$1.5M
Deleted in liver cancer 1 (DLC1) in liver development and diseaseK01DK097291 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SHIH, YI-PING · 2013 to 2016
$471k
NCI NIH HHS R01 CA151366NCI NIH HHS T32 CA108459NHLBI NIH HHS R01 HL070752NHLBI NIH HHS R01 HL126646NIDDK NIH HHS K01 DK097291
6 · The paper itself

Abstract

DLC1 is a RhoGAP-containing tumor suppressor that inhibits angiogenesis by repressing VEGF production in epithelial cells. Here we report the roles of DLC1 in endothelial cells. Silencing of DLC1 (siDLC1) enhances cell migration but reduces tube formation activities of human umbilical vein endothelial cells (HUVECs). Biochemically, RhoA activity and paxillin protein level are markedly increased in siDLC1 HUVECs. Although further silencing of RhoA restores the cell migration phenotype, the tube formation defect and up-regulated paxillin level remain unchanged. On the other hand, paxillin knockdown rescues tube formation and migration phenotypes but not the up-regulated RhoA activity. These results indicate that DLC1 regulates endothelial cell migration through RhoA and paxillin independently and controls tube formation mainly via paxillin. To further determine endothelial DLC1's function, we have generated endothelial specific knockout mice (DLC1-Tek). DLC1-Tek mice appear to be normal and healthy but their angiogenesis processes are compromised as shown in gel plug and aortic ring sprouting assays. Analysis of endothelial cells isolated from DLC1-Tek mice has further affirmed the cellular and biochemical phenotypes established in siDLC1 HUVECs. Our studies have demonstrated a positive regulatory role of endothelial DLC1 in angiogenesis.

Indexed as

Neovascularization, PhysiologicAnimalsCell MovementCells, CulturedDown-RegulationEndothelial CellsGenotypeGTPase-Activating ProteinsHumansHuman Umbilical Vein Endothelial CellsMice, KnockoutPaxillinPhenotyperhoA GTP-Binding Proteinrho GTP-Binding ProteinsRNA InterferenceDLC-1 (deleted in liver cancer) protein, mouseDLC1 protein, humanGTPase-Activating ProteinsPaxillinPXN protein, humanPxn protein, mouserhoA GTP-Binding ProteinRHOA protein, humanRhoA protein, mouserho GTP-Binding ProteinsTumor Suppressor ProteinsAngiogenesisDLC1Focal adhesionPaxillinRhoATube formation

Identifiers

PMID28408355
PMCPMC5460982
OpenAlexW2605457643

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.