Evidence map›Paper›PMID 24465899›Full record

ArticlePloS one2014

p120RasGAP is a mediator of rho pathway activation and tumorigenicity in the DLD1 colorectal cancer cell line.

Shawna L Organ, Josephine Hai, Nikolina Radulovich, Christopher B Marshall, Lisa Leung, Takehiko Sasazuki, Senji Shirasawa, Chang-Qi Zhu, Roya Navab, Mitsuhiko Ikura and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Clinical significance of theOncology letters · 2023
    Article
  2. Article
  3. Review
  4. Article
  5. p190RhoGAPs, theCells · 2019
    Review
  6. Article
  7. Article
  8. Article
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

11 authors at 4 institutions in 2 countries.

Shawna L OrganPrincess Margaret Cancer Centre, Toronto, Ontario, Canada ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Josephine HaiPrincess Margaret Cancer Centre, Toronto, Ontario, Canada ; Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Nikolina RadulovichPrincess Margaret Cancer Centre, Toronto, Ontario, Canada ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Christopher B MarshallPrincess Margaret Cancer Centre, Toronto, Ontario, Canada.
Lisa LeungPrincess Margaret Cancer Centre, Toronto, Ontario, Canada ; Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Takehiko SasazukiDepartment of Pathology, Research Institute, International Medical Center of Japan, Tokyo, Japan.
Senji ShirasawaDepartment of Cell Biology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Chang-Qi ZhuPrincess Margaret Cancer Centre, Toronto, Ontario, Canada.
Roya NavabPrincess Margaret Cancer Centre, Toronto, Ontario, Canada.
Mitsuhiko IkuraPrincess Margaret Cancer Centre, Toronto, Ontario, Canada ; Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Ming-Sound TsaoPrincess Margaret Cancer Centre, Toronto, Ontario, Canada ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada ; Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Princess Margaret Cancer Centre · CAUniversity of Toronto · CAFukuoka University · JPSaitama International Medical Center · JP

Funding

Canadian Institutes of Health Research MOP-64345
6 · The paper itself

Abstract

KRAS is mutated in ∼40% of colorectal cancer (CRC), and there are limited effective treatments for advanced KRAS mutant CRC. Therefore, it is crucial that downstream mediators of oncogenic KRAS continue to be studied. We identified p190RhoGAP as being phosphorylated in the DLD1 CRC cell line, which expresses a heterozygous KRAS G13D allele, and not in DKO4 in which the mutant allele has been deleted by somatic recombination. We found that a ubiquitous binding partner of p190RhoGAP, p120RasGAP (RasGAP), is expressed in much lower levels in DKO4 cells compared to DLD1, and this expression is regulated by KRAS. Rescue of RasGAP expression in DKO4 rescued Rho pathway activation and partially rescued tumorigenicity in DKO4 cells, indicating that the combination of mutant KRAS and RasGAP expression is crucial to these phenotypes. We conclude that RasGAP is an important effector of mutant KRAS in CRC.

Indexed as

Signal TransductionBase SequenceCarcinogenesisCell AdhesionCell Line, TumorCell MovementColorectal NeoplasmsGene Expression Regulation, NeoplasticGuanine Nucleotide Exchange FactorsHumansModels, BiologicalMolecular Sequence DataMutant ProteinsMutationp120 GTPase Activating ProteinPhenotypeARHGAP35 protein, humanGuanine Nucleotide Exchange FactorsKRAS protein, humanMutant Proteinsp120 GTPase Activating ProteinProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)RASA1 protein, humanras ProteinsRepressor ProteinsRNA, Messenger

Identifiers

PMID24465899
PMCPMC3897622
OpenAlexW2023435084

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.