Evidence map›Paper›PMID 24217116›Full record

ArticleCancers2013

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) Signaling Capacity and the Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer (NSCLC): Implications for Use of 1,25(OH)2D3 in NSCLC Treatment.

Santosh Kumar Upadhyay, Alissa Verone, Suzanne Shoemaker, Maochun Qin, Song Liu, Moray Campbell, Pamela A Hershberger

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Knockdown of CYP24A1 Aggravates 1α,25(OH)Frontiers in oncology · 2020
    Article
  13. Article
  14. Article
  15. Vitamin D Receptor Signaling and Cancer.Endocrinology and metabolism clinics of North America · 2017
    Review
  16. Article
  17. 1,25DOncotarget · 2017
    Article
  18. Article
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

Santosh Kumar UpadhyayDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA. pamela.hershberger@roswellpark.org.
Alissa Verone
Suzanne Shoemaker
Maochun Qin
Song Liu
Moray Campbell
Pamela A Hershberger
Roswell Park Comprehensive Cancer Center · US

Funding

Vitamin D3 Modulation of Inflammation and Lung Cancer RiskP50CA090440 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DACIC, SANJA · 2001 to 2015
$34.6M
DRUG DEVELOPMENT AND CANCER TREATMENTST32CA009072 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI JOHNSON, CANDACE S · 1985 to 2014
$2.3M
ROLE OF CYP24 IN NON-SMALL CELL LUNG CANCERR01CA132844 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HERSHBERGER, PAMELA A · 2009 to 2013
$1.4M
NCI NIH HHS P50 CA090440NCI NIH HHS R01 CA132844NCI NIH HHS T32 CA009072
6 · The paper itself

Abstract

1,25-dihydroxyvitamin D3 (1,25(OH)2D3) exerts anti-proliferative activity by binding to the vitamin D receptor (VDR) and regulating gene expression. We previously reported that non-small cell lung cancer (NSCLC) cells which harbor epidermal growth factor receptor (EGFR) mutations display elevated VDR expression (VDRhigh) and are vitamin D-sensitive. Conversely, those with K-ras mutations are VDRlow and vitamin D-refractory. Because EGFR mutations are found predominately in NSCLC cells with an epithelial phenotype and K-ras mutations are more common in cells with a mesenchymal phenotype, we investigated the relationship between vitamin D signaling capacity and the epithelial mesenchymal transition (EMT). Using NSCLC cell lines and publically available lung cancer cell line microarray data, we identified a relationship between VDR expression, 1,25(OH)2D3 sensitivity, and EMT phenotype. Further, we discovered that 1,25(OH)2D3 induces E-cadherin and decreases EMT-related molecules SNAIL, ZEB1, and vimentin in NSCLC cells. 1,25(OH)2D3-mediated changes in gene expression are associated with a significant decrease in cell migration and maintenance of epithelial morphology. These data indicate that 1,25(OH)2D3 opposes EMT in NSCLC cells. Because EMT is associated with increased migration, invasion, and chemoresistance, our data imply that 1,25(OH)2D3 may prevent lung cancer progression in a molecularly defined subset of NSCLC patients.

Identifiers

PMID24217116
PMCPMC3875951
OpenAlexW2008465434

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.