Evidence map›Paper›PMID 22992725›Full record

Trial reportThe Journal of biological chemistry2012

Elevated SP-1 transcription factor expression and activity drives basal and hypoxia-induced vascular endothelial growth factor (VEGF) expression in non-small cell lung cancer.

Karl Deacon, David Onion, Rajendra Kumari, Susan A Watson, Alan J Knox

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Long Noncoding RNA MALAT1: Salt-Sensitive Hypertension.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Sp1-mediated transcriptional regulation of MALAT1 plays a critical role in tumor.Journal of cancer research and clinical oncology · 2015
    Article
  15. Article
  16. Article
  17. Article
  18. MicroRNA-27b suppresses growth and invasion of NSCLC cells by targeting Sp1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    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

5 authors at 1 institution in 1 country.

Karl DeaconCentre for Respiratory Research, University of Nottingham, Nottingham, NG5 1PB, United Kingdom. karl.deacon@nottingham.ac.uk
David Onion
Rajendra Kumari
Susan A Watson
Alan J Knox
University of Nottingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

VEGF plays a central role in angiogenesis in cancer. Non-small cell lung cancer (NSCLC) tumors have increased microvascular density, localized hypoxia, and high VEGF expression levels; however, there is a lack of understanding of how oncogenic and tumor microenvironment changes such as hypoxia lead to greater VEGF expression in lung and other cancers. We show that NSCLC cells secreted higher levels of VEGF than normal airway epithelial cells. Actinomycin D inhibited all NSCLC VEGF secretion, and VEGF minimal promoter-luciferase reporter constructs were constitutively active until the last 85 base pairs before the transcription start site containing three SP-1 transcription factor-binding sites; mutation of these VEGF promoter SP-1-binding sites eliminated VEGF promoter activity. Furthermore, dominant negative SP-1, mithramycin A, and SP-1 shRNA decreased VEGF promoter activity, whereas overexpression of SP-1 increased VEGF promoter activity. Chromatin immunoprecipitation assays demonstrated SP-1, p300, and PCA/F histone acetyltransferase binding and histone H4 hyperacetylation at the VEGF promoter in NSCLC cells. Cultured NSCLC cells expressed higher levels of SP-1 protein than normal airway epithelial cells, and double-fluorescence immunohistochemistry showed a strong correlation between SP-1 and VEGF in human NSCLC tumors. In addition, hypoxia-driven VEGF expression in NSCLC cells was SP-1-dependent, with hypoxia increasing SP-1 activity and binding to the VEGF promoter. These studies are the first to demonstrate that overexpression of SP-1 plays a central role in hypoxia-induced VEGF secretion.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Non-Small-Cell LungCell HypoxiaCell Line, TumorDactinomycinFemaleHistonesHumansHypoxiaLung NeoplasmsMaleNeoplasm ProteinsNeovascularization, PathologicNucleic Acid Synthesis Inhibitorsp300-CBP-Associated Factorp300-CBP Transcription FactorsDactinomycinHistonesNeoplasm ProteinsNucleic Acid Synthesis Inhibitorsp300-CBP-Associated Factorp300-CBP Transcription FactorsSp1 Transcription FactorVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID22992725
PMCPMC3501049
OpenAlexW2059350051

What OpenQuestion holds

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LicenceCC BY-NC
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.