Evidence map›Paper›PMID 38916963›Full record

ArticleJCI insight2024

HPV8-induced STAT3 activation led keratinocyte stem cell expansion in human actinic keratoses.

Huw J Morgan, Carlotta Olivero, Boris Y Shorning, Alex Gibbs, Alexandra L Phillips, Lokapriya Ananthan, Annabelle Xiao Hui Lim, Licia Martuscelli, Cinzia Borgogna, Marco De Andrea and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

15 authors.

Huw J MorganEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Carlotta OliveroEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Boris Y ShorningEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Alex GibbsEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Alexandra L PhillipsEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Lokapriya AnanthanEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Annabelle Xiao Hui LimEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Licia MartuscelliDepartment of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Cinzia BorgognaDepartment of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Marco De AndreaViral Pathogenesis Unit, Department of Public Health and Pediatric Sciences, University of Turin Medical School, Turin, Italy.
Martin HufbauerInstitute of Virology, University of Cologne, Medical Faculty and University Hospital Cologne, Cologne, Germany.
Richard GoodwinDepartment of Dermatology, Aneurin Bevan University Health Board, Royal Gwent Hospital, Newport, United Kingdom.
Baki AkgülInstitute of Virology, University of Cologne, Medical Faculty and University Hospital Cologne, Cologne, Germany.
Marisa GariglioDepartment of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Girish K PatelEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite epidermal turnover, the skin is host to a complex array of microbes, including viruses, such as HPV, which must infect and manipulate skin keratinocyte stem cells (KSCs) to survive. This crosstalk between the virome and KSC populations remains largely unknown. Here, we investigated the effect of HPV8 on KSCs using various mouse models. We observed that the HPV8 early region gene E6 specifically caused Lrig1+ hair follicle junctional zone KSC proliferation and expansion, which would facilitate viral transmission. Within Lrig1+ KSCs specifically, HPV8 E6 bound intracellular p300 to phosphorylate the STAT3 transcriptional regulatory node. This induced ΔNp63 expression, resulting in KSC expansion into the overlying epidermis. HPV8 was associated with 70% of human actinic keratoses. Together, these results define the "hit-and-run" mechanism for HPV8 in human actinic keratosis as an expansion of KSCs, which lack melanosome protection and are thus susceptible to sun light-induced malignant transformation.

Indexed as

Cell ProliferationKeratinocytesKeratosis, ActinicOncogene Proteins, ViralPapillomavirus InfectionsSTAT3 Transcription FactorStem CellsAnimalsDisease Models, AnimalFemaleHumansMiceE6 protein, Human papillomavirus type 8Oncogene Proteins, ViralSTAT3 protein, humanSTAT3 Transcription FactorAdult stem cellsCell biologyMouse modelsSkin cancerStem cells

Identifiers

PMID38916963
PMCPMC11383611

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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.