Evidence map›Paper›PMID 27918748›Full record

ArticlePLoS pathogens2016

The CXCL12/CXCR4 Signaling Pathway: A New Susceptibility Factor in Human Papillomavirus Pathogenesis.

Floriane Meuris, Laetitia Carthagena, Agnieszka Jaracz-Ros, Françoise Gaudin, Pasquale Cutolo, Claire Deback, Yuezhen Xue, Françoise Thierry, John Doorbar, Françoise Bachelerie

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 44 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 3 countries.

Floriane MeurisInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.
Laetitia CarthagenaInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.
Agnieszka Jaracz-RosInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.
Françoise GaudinInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.
Pasquale CutoloInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.
Claire DebackInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.ORCID http://orcid.org/0000-0001-9465-2381
Yuezhen XuePapillomavirus Regulation and Cancer, Institute of Medical Biology, A*STAR, Singapore.
Françoise ThierryPapillomavirus Regulation and Cancer, Institute of Medical Biology, A*STAR, Singapore.
John DoorbarDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom.
Françoise BachelerieInflammation Chemokines and Immunopathology, INSERM, Fac. de médecine-Univ Paris-Sud, Université Paris-Saclay, Clamart, France.
Inserm · FRAgency for Science, Technology and Research · SGCentre National de la Recherche Scientifique · FRUniversity of Cambridge · GB

Funding

Medical Research Council MC_PC_13050
6 · The paper itself

Abstract

The productive human papillomavirus (HPV) life cycle is tightly linked to the differentiation and cycling of keratinocytes. Deregulation of these processes and stimulation of cell proliferation by the action of viral oncoproteins and host cell factors underlies HPV-mediated carcinogenesis. Severe HPV infections characterize the wart, hypogammaglobulinemia, infection, and myelokathexis (WHIM) immunodeficiency syndrome, which is caused by gain-of-function mutations in the CXCR4 receptor for the CXCL12 chemokine, one of which is CXCR41013. We investigated whether CXCR41013 interferes in the HPV18 life cycle in epithelial organotypic cultures. Expression of CXCR41013 promoted stabilization of HPV oncoproteins, thus disturbing cell cycle progression and proliferation at the expense of the ordered expression of the viral genes required for virus production. Conversely, blocking CXCR41013 function restored virus production and limited HPV-induced carcinogenesis. Thus, CXCR4 and its potential activation by genetic alterations in the course of the carcinogenic process can be considered as an important host factor for HPV carcinogenesis.

Indexed as

Signal TransductionAnimalsBlotting, WesternCell LineCell Transformation, ViralChemokine CXCL12Genetic Predisposition to DiseaseHeterograftsHuman papillomavirus 18KeratinocytesMiceMice, NudePapillomavirus InfectionsReceptors, CXCR4Skin NeoplasmsChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanReceptors, CXCR4

Identifiers

PMID27918748
PMCPMC5138052
OpenAlexW2559817135

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.