Evidence map›Paper›PMID 31825828›Full record

ArticleCell reports2019

DIRAS3 (ARHI) Blocks RAS/MAPK Signaling by Binding Directly to RAS and Disrupting RAS Clusters.

Margie N Sutton, Zhen Lu, Yao-Cheng Li, Yong Zhou, Tao Huang, Albert S Reger, Amy M Hurwitz, Timothy Palzkill, Craig Logsdon, Xiaowen Liang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  5. Statins inhibit onco-dimerization of the 4Ig isoform of B7-H3.bioRxiv : the preprint server for biology · 2024
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  12. Expression ofInternational journal of molecular sciences · 2024
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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

15 authors at 5 institutions in 1 country.

Margie N SuttonDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Zhen LuDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Yao-Cheng LiGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Yong ZhouDepartment of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, TX 77030, USA.
Tao HuangDepartment of Biomedical Engineering, Oregon Health & Science University, Portland, OR 97201, USA.
Albert S RegerDepartment of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Amy M HurwitzDepartment of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Timothy PalzkillDepartment of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Craig LogsdonDepartment of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Xiaowen LiangDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Joe W GrayDepartment of Biomedical Engineering, Oregon Health & Science University, Portland, OR 97201, USA.
Xiaolin NanDepartment of Biomedical Engineering, Oregon Health & Science University, Portland, OR 97201, USA.
John HancockDepartment of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, TX 77030, USA.
Geoffrey M WahlGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Robert C BastDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: rbast@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USOregon Health & Science University · USSalk Institute for Biological Studies · USThe University of Texas Health Science Center at Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Convalescent Plasma to Limit Coronavirus Associated ComplicationsUL1TR003167 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KARP, DANIEL D, MCPHERSON, DAVID D · 2019 to 2023
$45.3M
UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
Center for Clinical and Translational Sciences (CCTS)UL1TR000371 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2012 to 2016
$13.4M
U.T. M. D. Anderson Cancer Center SPORE in Ovarian CancerP50CA217685 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2017 to 2021
$7.9M
Combining single cell approaches and a developmental perspective to discover stem cell control circuits and the cellular and molecular bases of cancer heterogeneityR35CA197687 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI WAHL, GEOFFREY MYLES · 2015 to 2021
$7.8M
Supplement to CA135354 "ARHI (DIRAS3) in Autophagy and Dormancy of Ovarian Cancer"R01CA135354 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 2009 to 2019
$3.5M
Center for Clinical and Translational Sciences (CCTS)TL1TR000369 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2012 to 2016
$1.9M
NCATS NIH HHS TL1 TR000369NCATS NIH HHS UL1 TR000371NCATS NIH HHS UL1 TR003167NCI NIH HHS P30 CA014195NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA083639NCI NIH HHS P50 CA217685NCI NIH HHS R01 CA135354NCI NIH HHS R35 CA197687
6 · The paper itself

Abstract

Oncogenic RAS mutations drive cancers at many sites. Recent reports suggest that RAS dimerization, multimerization, and clustering correlate strongly with activation of RAS signaling. We have found that re-expression of DIRAS3, a RAS-related small GTPase tumor suppressor that is downregulated in multiple cancers, inhibits RAS/mitogen-activated protein kinase (MAPK) signaling by interacting directly with RAS-forming heteromers, disrupting RAS clustering, inhibiting Raf kinase activation, and inhibiting transformation and growth of cancer cells and xenografts. Disruption of K-RAS cluster formation requires the N terminus of DIRAS3 and interaction of both DIRAS3 and K-RAS with the plasma membrane. Interaction of DIRAS3 with both K-RAS and H-RAS suggests a strategy for inhibiting oncogenic RAS function.

Indexed as

MAP Kinase Signaling System3T3 CellsAnimalsCarcinogenesisCell Line, TumorFemaleHumansMiceMice, NudeProtein BindingProto-Oncogene Proteins p21(ras)raf Kinasesrho GTP-Binding ProteinsDIRAS3 protein, humanHRAS protein, humanKRAS protein, humanProto-Oncogene Proteins p21(ras)raf Kinasesrho GTP-Binding ProteinsARHIclusterdimerDIRAS3heteromerovarian cancerpancreatic cancerRAS inhibitortransformation

Identifiers

PMID31825828
PMCPMC6948147
OpenAlexW2995284457

What OpenQuestion holds

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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.