Evidence map›Paper›PMID 32641858›Full record

ArticleOncogene2020

p190A RhoGAP induces CDH1 expression and cooperates with E-cadherin to activate LATS kinases and suppress tumor cell growth.

Hanyue Ouyang, Phi Luong, Morten Frödin, Steen H Hansen

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
  2. Article
  3. Article
  4. The mCell death discovery · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Hippo Signaling in the Endometrium.International journal of molecular sciences · 2022
    Review
  11. 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

4 authors at 2 institutions in 2 countries.

Hanyue OuyangGI Cell Biology Laboratory, Boston Children's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Phi LuongGI Cell Biology Laboratory, Boston Children's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Morten FrödinBiotech Research & Innovation Centre (BRIC), University of Copenhagen, 2200, Copenhagen N, Denmark.
Steen H HansenGI Cell Biology Laboratory, Boston Children's Hospital and Harvard Medical School, Boston, MA, 02115, USA. steen.hansen@childrens.harvard.edu.ORCID http://orcid.org/0000-0002-9408-4676
Boston Children's Hospital · USUniversity of Copenhagen · DK

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI JONATHAN C KAGAN · 1986 to 2026
$32.4M
p190 RhoGAP signaling in epithelial oncogenesisR01CA205158 · NCI · BOSTON CHILDREN'S HOSPITAL · PI HANSEN, STEEN HENNING · 2017 to 2021
$2.0M
NCI NIH HHS R01 CA205158NIDDK NIH HHS P30 DK034854
6 · The paper itself

Abstract

The ARHGAP35 gene encoding p190A RhoGAP (p190A) is significantly altered by both mutation and allelic deletion in human cancer, but the functional implications of such alterations are not known. Here, we demonstrate for the first time that p190A is a tumor suppressor using a xenograft mouse model with carcinoma cells harboring defined ARHGAP35 alterations. In vitro, restoration of p190A expression in carcinoma cells promotes contact inhibition of proliferation (CIP) through activation of LATS kinases and phosphorylation of the proto-oncogenic transcriptional co-activator YAP. In contrast, p190A forms harboring recurrent cancer mutations exhibit loss of function in modulating the Hippo pathway, inducing CIP, as well as attenuated suppression of tumor growth in mice. We determine that p190A promotes mesenchymal to epithelial transition (MET) and elicits expression of a cassette of epithelial adherens junction-associated genes in a cell density-dependent manner. This cassette includes CDH1 encoding E-cadherin, which amplifies p190A-mediated LATS activation and is necessary for CIP. Oppositely, we establish that p190A is obligatory for E-cadherin to activate LATS kinases and induce CIP. Collectively, this work defines a novel mechanism by which p190A and E-cadherin cooperate in modulating Hippo signaling to suppress tumor cell growth.

Indexed as

AnimalsAntigens, CDCadherinsCell Growth ProcessesCell Line, TumorEnzyme ActivationFemaleGuanine Nucleotide Exchange FactorsHEK293 CellsHeLa CellsHumansMiceMice, NudeNeoplasmsProtein Serine-Threonine KinasesRepressor ProteinsAntigens, CDARHGAP35 protein, humanCadherinsCDH1 protein, humanGuanine Nucleotide Exchange FactorsProtein Serine-Threonine KinasesRepressor Proteins

Identifiers

PMID32641858
PMCPMC7426264
OpenAlexW3041145084

What OpenQuestion holds

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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.