Evidence map›Paper›PMID 25413277›Full record

ArticleNature communications2014

RHOA inactivation enhances Wnt signalling and promotes colorectal cancer.

Paulo Rodrigues, Irati Macaya, Sarah Bazzocco, Rocco Mazzolini, Elena Andretta, Higinio Dopeso, Silvia Mateo-Lozano, Josipa Bilić, Fernando Cartón-García, Rocio Nieto and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 111 citations in OpenAlex.

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3 more citing papers are in PubMed but not listed here.

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

21 authors at 7 institutions in 3 countries.

Paulo Rodrigues1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Irati Macaya1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Sarah Bazzocco1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Rocco Mazzolini1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Elena Andretta1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Higinio Dopeso1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Silvia Mateo-Lozano1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Josipa Bilić1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Fernando Cartón-García1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Rocio Nieto1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Lucia Suárez-López1] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain [2] Group of Drug Delivery and Targeting, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain.
Elsa Afonso1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
Stefania LandolfiDepartment of Pathology, Vall d'Hebron Hospital, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain.
Javier Hernandez-LosaDepartment of Pathology, Vall d'Hebron Hospital, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain.
Kazuto KobayashiDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan.
Santiago Ramón y CajalDepartment of Pathology, Vall d'Hebron Hospital, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain.
Josep TaberneroDepartment of Medical Oncology, Vall d'Hebron University Hospital and Institute of Oncology (VHIO), Universitat Autònoma de Barcelona, 119-129, Barcelona 08035, Spain.
Niall C TebbuttLudwig Institute for Cancer Research, Melbourne-Branch, Austin Health, Heidelberg, Victoria 3084, Australia.
John M MariadasonLudwig Institute for Cancer Research, Melbourne-Branch, Austin Health, Heidelberg, Victoria 3084, Australia.
Simo Schwartz1] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain [2] Group of Drug Delivery and Targeting, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain.
Diego Arango1] Group of Molecular Oncology, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Passeig Vall d'Hebron, 119-129, Barcelona 08035, Spain [2] CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Barcelona, Spain.
CIBBIM-Nanomedicine · ESBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESUniversitat Autònoma de Barcelona · ESVall d'Hebron Hospital Universitari · ESAustin Health · AUFukushima Medical University · JPLudwig Cancer Research · AU

Funding

Worldwide Cancer Research 13-0245
6 · The paper itself

Abstract

Activation of the small GTPase RHOA has strong oncogenic effects in many tumour types, although its role in colorectal cancer remains unclear. Here we show that RHOA inactivation contributes to colorectal cancer progression/metastasis, largely through the activation of Wnt/β-catenin signalling. RhoA inactivation in the murine intestine accelerates the tumorigenic process and in human colon cancer cells leads to the redistribution of β-catenin from the membrane to the nucleus and enhanced Wnt/β-catenin signalling, resulting in increased proliferation, invasion and de-differentiation. In mice, RHOA inactivation contributes to colon cancer metastasis and reduced RHOA levels were observed at metastatic sites compared with primary human colon tumours. Therefore, we have identified a new mechanism of activation of Wnt/β-catenin signalling and characterized the role of RHOA as a novel tumour suppressor in colorectal cancer. These results constitute a shift from the current paradigm and demonstrate that RHO GTPases can suppress tumour progression and metastasis.

Indexed as

Gene SilencingSignal TransductionAnimalsbeta CateninCell Line, TumorColonic NeoplasmsDisease ProgressionGene Expression Regulation, NeoplasticHumansMicerhoA GTP-Binding ProteinWnt Proteinsbeta CateninrhoA GTP-Binding ProteinRHOA protein, humanWnt Proteins

Identifiers

PMID25413277
PMCPMC4255233
OpenAlexW2047283612

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Registered trials

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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.