Evidence map›Paper›PMID 26068789›Full record

ArticleCell death & disease2015

1α, 25-Dihydroxyvitamin D₃ and the vitamin D receptor regulates ΔNp63α levels and keratinocyte proliferation.

N T Hill, J Zhang, M K Leonard, M Lee, H N Shamma, M Kadakia

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Vitamin D receptor cross-talk with p63 signaling promotes epidermal cell fate.The Journal of steroid biochemistry and molecular biology · 2023
    Article
  6. Role of vitamin D and calcium signaling in epidermal wound healing.Journal of endocrinological investigation · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
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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

6 authors at 1 institution in 1 country.

N T HillDepartment of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA.
J ZhangDepartment of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA.
M K LeonardDepartment of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA.
M Lee1] Lifespan Health Research Center, Department of Community Health, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA [2] Department of Pediatrics, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA.
H N ShammaDepartment of Dermatology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA.
M KadakiaDepartment of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH, USA.
Wright State University · US

Funding

Role of DeltaNp63alpha in Vitamin D Mediated Cell Survival in Skin CancerR01CA154715 · NCI · WRIGHT STATE UNIVERSITY · PI KADAKIA, MADHAVI P · 2012 to 2016
$1.4M
NCI NIH HHS 1R01CA154715NCI NIH HHS R01 CA154715
6 · The paper itself

Abstract

1α, 25-dihydroxyvitamin D3 (VD3), a secosteriod that has been explored as an anti-cancer agent, was also shown to promote cell survival. Its receptor, the Vitamin D Receptor (VDR), is a direct target of the proto-oncogene ΔNp63α, which is overexpressed in non-melanoma skin cancers. The interconnection between VDR/VD3 signaling and ΔNp63α, led us to examine whether VDR/VD3 signaling promotes keratinocyte proliferation by regulating ΔNp63α levels. Our data demonstrate that VDR regulates ΔNp63α expression at both the transcript and protein level. Interestingly, although low doses of VD3 led to an increase in ΔNp63α protein levels and keratinocyte proliferation, high doses of VD3 failed to increase ΔNp63α protein levels and resulted in reduced proliferation. Increased expression of ΔNp63α by low dose VD3 was shown to be dependent on VDR and critical for the proliferative effects of VD3. VD3-mediated increases in ΔNp63α protein levels occur via activation of both p38 MAPK and Akt kinases. Finally, analysis of samples from patients with squamous cell carcinoma (SCC), basal cell carcinoma and precursors to invasive SCC demonstrated a significant correlation between p63 and VDR levels when compared with healthy normal skin control samples. Delineation of the mechanisms by which VD3 exerts its effect on ΔNp63α and cell proliferation is critical for determining the future of VD3 in cancer therapies.

Indexed as

Basal Cell CarcinomaCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell SurvivalCholecalciferolHeterocyclic Compounds, 3-RingHumansImidazolesKeratinocytesNaphthalenesp38 Mitogen-Activated Protein KinasesPhenylurea CompoundsProto-Oncogene MasProto-Oncogene Proteins c-aktPyrazoles4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleCholecalciferoldoramapimodHeterocyclic Compounds, 3-RingImidazolesMAS1 protein, humanMK 2206Naphthalenesp38 Mitogen-Activated Protein KinasesPhenylurea CompoundsProto-Oncogene MasProto-Oncogene Proteins c-aktPyrazolesPyridinesReceptors, CalcitriolRNA, Small InterferingTP63 protein, humanTranscription FactorsTumor Suppressor ProteinsVDR protein, human

Identifiers

PMID26068789
PMCPMC4669830
OpenAlexW2431410296

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.