Evidence map›Paper›PMID 30452903›Full record

ReviewThe Journal of investigative dermatology2019

Collagen Prolyl Hydroxylases Are Bifunctional Growth Regulators in Melanoma.

Aithne Atkinson, Alexander Renziehausen, Hexiao Wang, Cristiana Lo Nigro, Laura Lattanzio, Marco Merlano, Bhavya Rao, Lynda Weir, Alan Evans, Rubeta Matin and 13 more

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of investigative dermatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  6. Collagen IV biosynthesis: Intracellular choreography of post-translational modifications.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
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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

23 authors at 14 institutions in 5 countries.

Aithne AtkinsonJohn Fulcher Brain Tumour Research Laboratory, Imperial College, Hammersmith Hospital, London, UK.
Alexander RenziehausenJohn Fulcher Brain Tumour Research Laboratory, Imperial College, Hammersmith Hospital, London, UK.
Hexiao WangDepartment of Dermatology, The First Hospital of China Medical University, Shenyang, China.
Cristiana Lo NigroLaboratory of Cancer Genetics and Translational Oncology, S. Croce General Hospital, Cuneo, Italy.
Laura LattanzioLaboratory of Cancer Genetics and Translational Oncology, S. Croce General Hospital, Cuneo, Italy.
Marco MerlanoLaboratory of Cancer Genetics and Translational Oncology, S. Croce General Hospital, Cuneo, Italy.
Bhavya RaoDundee Cancer Centre, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Lynda WeirDundee Cancer Centre, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Alan EvansDepartment of Pathology, Ninewells Hospital, Dundee, UK.
Rubeta MatinBarts and the London School of Medicine and Dentistry, Queen Mary University of London, Imperial College London, London, UK.
Catherine HarwoodBarts and the London School of Medicine and Dentistry, Queen Mary University of London, Imperial College London, London, UK.
Peter SzlosarekBarts and the London School of Medicine and Dentistry, Queen Mary University of London, Imperial College London, London, UK.
J Geoffrey PickeringRobarts Research Institute, Western University, London, Ontario, Canada.
Colin FlemingDepartment of Dermatology, Ninewells Hospital, Dundee, UK.
Van Ren SimKent Oncology Centre, Maidstone Hospital, Maidstone, UK.
Su LiRoyal Marsden Hospital, Fulham Road, London, UK.
James T VastaDepartment of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Ronald T RainesDepartment of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA; Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Mathieu BoniolInternational Prevention Research Institute, Lyon, France.
Alastair ThompsonMD Anderson Cancer Center, Houston, Texas, USA.
Charlotte ProbyDundee Cancer Centre, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK; Department of Dermatology, Ninewells Hospital, Dundee, UK.
Tim CrookDepartment of Oncology, St Luke's Cancer Centre, Royal Surrey County Hospital, Guilford, UK. Electronic address: timothycrook@nhs.net.
Nelofer SyedJohn Fulcher Brain Tumour Research Laboratory, Imperial College, Hammersmith Hospital, London, UK. Electronic address: n.syed@imperial.ac.uk.
Ninewells Hospital · GBBrain Tumour Research · GBImperial College London · GBUniversity of Dundee · GBUniversity of Wisconsin–Madison · USChina Medical University · CNHammersmith Hospital · GBInternational Prevention Research Institute · FRMaidstone Hospital · GBQueen Mary University of London · GBRoyal Marsden Hospital · GBRoyal Surrey County Hospital · GBThe University of Texas MD Anderson Cancer Center · USWestern University · CA

Funding

COLLAGEN STRUCTURE AND STABILITY IN VITRO AND IN VIVOR01AR044276 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI RAINES, RONALD T · 1996 to 2017
$5.6M
Cancer Research UKChief Scientist OfficeMedical Research CouncilNIAMS NIH HHS R01 AR044276
6 · The paper itself

Abstract

Appropriate post-translational processing of collagen requires prolyl hydroxylation, catalyzed by collagen prolyl 3-hydroxylase and collagen prolyl 4-hydroxylase, and is essential for normal cell function. Here we have investigated the expression, transcriptional regulation, and function of the collagen prolyl 3-hydroxylase and collagen prolyl 4-hydroxylase families in melanoma. We show that the collagen prolyl 3-hydroxylase family exemplified by Leprel1 and Leprel2 is subject to methylation-dependent transcriptional silencing in primary and metastatic melanoma consistent with a tumor suppressor function. In contrast, although there is transcriptional silencing of P4HA3 in a subset of melanomas, the collagen prolyl 4-hydroxylase family members P4HA1, P4HA2, and P4HA3 are often overexpressed in melanoma, expression being prognostic of worse clinical outcomes. Consistent with tumor suppressor function, ectopic expression of Leprel1 and Leprel2 inhibits melanoma proliferation, whereas P4HA2 and P4HA3 increase proliferation, and particularly invasiveness, of melanoma cells. Pharmacological inhibition with multiple selective collagen prolyl 4-hydroxylase inhibitors reduces proliferation and inhibits invasiveness of melanoma cells. Together, our data identify the collagen prolyl 3-hydroxylase and collagen prolyl 4-hydroxylase families as potentially important regulators of melanoma growth and invasiveness and suggest that selective inhibition of collagen prolyl 4-hydroxylase is an attractive strategy to reduce the invasive properties of melanoma cells.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorCell ProliferationCollagenDNA MethylationHumansMelanomaProcollagen-Proline DioxygenaseProlyl HydroxylasesProtein Processing, Post-TranslationalReference ValuesSkin NeoplasmsCollagenP3H2 protein, humanProcollagen-Proline DioxygenaseProlyl Hydroxylases

Identifiers

PMID30452903
PMCPMC7015666
OpenAlexW2900617033

What OpenQuestion holds

Textmetadata
LicenceTDM
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.