Evidence map›Paper›PMID 28460460›Full record

ArticleOncotarget2017

Clinical relevance of the transcriptional signature regulated by CDC42 in colorectal cancer.

Fatima Valdés-Mora, Warwick J Locke, Eva Bandrés, David Gallego-Ortega, Paloma Cejas, Miguel Angel García-Cabezas, Yolanda Colino-Sanguino, Jaime Feliú, Teresa Gómez Del Pulgar, Juan Carlos Lacal

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 19 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

10 authors at 4 institutions in 2 countries.

Fatima Valdés-MoraHistone Variants Group, Epigenetics Research Program, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Warwick J LockeEpigenetics Research Program, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Eva BandrésImmunology Unit, Department of Haematology, Complejo Hospitalario de Navarra, Navarra Health Service, Pamplona, Spain.
David Gallego-OrtegaSt. Vincent's Clinical School, Faculty of Medicine, University of New South Wales Sydney, New South Wales, Australia.
Paloma CejasLaboratorio de Oncología Translacional, Servicio de Oncología Médica, IdiPAZ, Madrid, Spain.
Miguel Angel García-CabezasServicio de Anatomía Patológica, Hospital Universitario La Paz, Madrid, Spain.
Yolanda Colino-SanguinoHistone Variants Group, Epigenetics Research Program, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Jaime FeliúLaboratorio de Oncología Translacional, Servicio de Oncología Médica, IdiPAZ, Madrid, Spain.
Teresa Gómez Del PulgarLaboratorio de Oncología Translacional, Servicio de Oncología Médica, IdiPAZ, Madrid, Spain.
Juan Carlos LacalLaboratorio de Oncología Translacional, Servicio de Oncología Médica, IdiPAZ, Madrid, Spain.
Garvan Institute of Medical Research · AUCentro de Investigación Biomédica en Red de Cáncer · ESComplejo Hospitalario de Navarra · ESHospital Universitario La Paz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CDC42 is an oncogenic Rho GTPase overexpressed in colorectal cancer (CRC). Although CDC42 has been shown to regulate gene transcription, the specific molecular mechanisms regulating the oncogenic ability of CDC42 remain unknown. Here, we have characterized the transcriptional networks governed by CDC42 in the CRC SW620 cell line using gene expression analysis. Our results establish that several cancer-related signaling pathways, including cell migration and cell proliferation, are regulated by CDC42. This transcriptional signature was validated in two large cohorts of CRC patients and its clinical relevance was also studied. We demonstrate that three CDC42-regulated genes offered a better prognostic value when combined with CDC42 compared to CDC42 alone. In particular, the concordant overexpression of CDC42 and silencing of the putative tumor suppressor gene CACNA2D2 dramatically improved the prognostic value. The CACNA2D2/CDC42 prognostic classifier was further validated in a third CRC cohort as well as in vitro and in vivo CRC models. Altogether, we show that CDC42 has an active oncogenic role in CRC via the transcriptional regulation of multiple cancer-related pathways and that CDC42-mediated silencing of CACNA2D2 is clinically relevant. Our results further support the use of CDC42 specific inhibitors for the treatment of the most aggressive types of CRC.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptomeAnimalsCalcium Channelscdc42 GTP-Binding ProteinCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsDisease Models, AnimalFemaleGene Expression ProfilingGene Regulatory NetworksGenes, Tumor SuppressorHeterograftsHumansCACNA2D2 protein, humanCalcium Channelscdc42 GTP-Binding ProteinCACNA2D2CDC42colorectal cancerprognostic factortumor suppressor genes

Identifiers

PMID28460460
PMCPMC5432295
OpenAlexW2593033216

What OpenQuestion holds

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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.