Evidence map›Paper›PMID 29206819›Full record

ArticleBritish journal of cancer2018

Mechanisms of inactivation of the tumour suppressor gene RHOA in colorectal cancer.

Higinio Dopeso, Paulo Rodrigues, Josipa Bilic, Sarah Bazzocco, Fernando Cartón-García, Irati Macaya, Priscila Guimarães de Marcondes, Estefanía Anguita, Marc Masanas, Lizbeth M Jiménez-Flores and 6 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

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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

16 authors at 5 institutions in 2 countries.

Higinio DopesoGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Paulo RodriguesGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Josipa BilicGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Sarah BazzoccoGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Fernando Cartón-GarcíaGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Irati MacayaGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Priscila Guimarães de MarcondesGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Estefanía AnguitaGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Marc MasanasLaboratory of Translational Research in Child and Adolescent Cancer, Vall d'Hebron Research Institute (VHIR)-UAB, Barcelona 08035, Spain.
Lizbeth M Jiménez-FloresGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Águeda Martínez-BarriocanalGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Rocío NietoGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Miguel F SeguraLaboratory of Translational Research in Child and Adolescent Cancer, Vall d'Hebron Research Institute (VHIR)-UAB, Barcelona 08035, Spain.
Simo SchwartzDrug Delivery and Targeting Group, CIBBIM Nanomedicine, Vall d'Hebron Research Institute (VHIR), Barcelona 08035, Spain.
John M MariadasonLa Trobe University School of Cancer Medicine, Olivia Newton-John Cancer Research Institute, Melbourne 3084, VIC, Australia.
Diego ArangoGroup of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain.
Vall d'Hebron Institut de Recerca · ESCIBBIM-Nanomedicine · ESUniversitat Autònoma de Barcelona · ESBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESLa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundReduced RHOA signalling has been shown to increase the growth/metastatic potential of colorectal tumours. However, the mechanisms of inactivation of RHOA signalling in colon cancer have not been characterised.

methodsA panel of colorectal cancer cell lines and large cohorts of primary tumours were used to investigate the expression and activity of RHOA, as well as the presence of RHOA mutations/deletions and promoter methylation affecting RHOA. Changes in RHOA expression were assessed by western blotting and qPCR after modulation of microRNAs, SMAD4 and c-MYC.

resultsWe show here that RHOA point mutations and promoter hypermethylation do not significantly contribute to the large variability of RHOA expression observed among colorectal tumours. However, RHOA copy number loss was observed in 16% of colorectal tumours and this was associated with reduced RHOA expression. Moreover, we show that miR-200a/b/429 downregulates RHOA in colorectal cancer cells. In addition, we found that TGF-β/SMAD4 upregulates the RHOA promoter. Conversely, RHOA expression is transcriptionally downregulated by canonical Wnt signalling through the Wnt target gene c-MYC that interferes with the binding of SP1 to the RHOA promoter in colon cancer cells.

conclusionsWe demonstrate a complex pattern of inactivation of the tumour suppressor gene RHOA in colon cancer cells through genetic, transcriptional and post-transcriptional mechanisms.

Indexed as

DNA Copy Number VariationsDown-RegulationCell Line, TumorCohort StudiesColorectal NeoplasmsDNA MethylationFemaleGene DosageGene Expression Regulation, NeoplasticHumansMaleMicroRNAsPoint MutationProto-Oncogene Proteins c-mycrhoA GTP-Binding ProteinSignal TransductionMicroRNAsMIRN200 microRNA, humanMIRN429 microRNA, humanMYC protein, humanProto-Oncogene Proteins c-mycrhoA GTP-Binding ProteinRHOA protein, humanSmad4 ProteinSMAD4 protein, human

Identifiers

PMID29206819
PMCPMC5765235
OpenAlexW2775577499

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.