Evidence map›Paper›PMID 23426183›Full record

ArticleThe Journal of clinical investigation2013

Cigarette smoke mediates epigenetic repression of miR-487b during pulmonary carcinogenesis.

Sichuan Xi, Hong Xu, Jigui Shan, Yongguang Tao, Julie A Hong, Suzanne Inchauste, Mary Zhang, Tricia F Kunst, Leandro Mercedes, David S Schrump

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing 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

77 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).Journal of toxicology and environmental health. Part B, Critical reviews · 2023
    Review
  9. Article
  10. CRISPR-Cas9-mediated gene therapy in lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. NCancer communications (London, England) · 2021
    Review
  18. Review
  19. Article
  20. Review

17 more citing papers are in PubMed but not listed here.

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

10 authors.

Sichuan XiThoracic Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA.
Hong Xu
Jigui Shan
Yongguang Tao
Julie A Hong
Suzanne Inchauste
Mary Zhang
Tricia F Kunst
Leandro Mercedes
David S Schrump

Funding

Modulating Cancer Stem Cell Signaling in Thoracic MalignanciesZIABC011418 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHRUMP, DAVID · 2011 to 2025
$17.4M
Epigenetic Mechanisms of Gene Expression in Thoracic MalignanciesZIABC011115 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHRUMP, DAVID · 2009 to 2025
$15.1M
Epigenetic Alterations Induced by Tobacco SmokeZIABC011122 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHRUMP, DAVID · 2009 to 2013
$3.3M
Intramural NIH HHS ZIA BC011122Intramural NIH HHS ZIA BC011418
6 · The paper itself

Abstract

MicroRNAs are critical mediators of stem cell pluripotency, differentiation, and malignancy. Limited information exists regarding microRNA alterations that facilitate initiation and progression of human lung cancers. In this study, array techniques were used to evaluate microRNA expression in normal human respiratory epithelia and lung cancer cells cultured in the presence or absence of cigarette smoke condensate (CSC). Under relevant exposure conditions, CSC significantly repressed miR-487b. Subsequent experiments demonstrated that miR-487b directly targeted SUZ12, BMI1, WNT5A, MYC, and KRAS. Repression of miR-487b correlated with overexpression of these targets in primary lung cancers and coincided with DNA methylation, de novo nucleosome occupancy, and decreased H2AZ and TCF1 levels within the miR-487b genomic locus. Deoxy-azacytidine derepressed miR-487b and attenuated CSC-mediated silencing of miR-487b. Constitutive expression of miR-487b abrogated Wnt signaling, inhibited in vitro proliferation and invasion of lung cancer cells mediated by CSC or overexpression of miR-487b targets, and decreased growth and metastatic potential of lung cancer cells in vivo. Collectively, these findings indicate that miR-487b is a tumor suppressor microRNA silenced by epigenetic mechanisms during tobacco-induced pulmonary carcinogenesis and suggest that DNA demethylating agents may be useful for activating miR-487b for lung cancer therapy.

Indexed as

RNA InterferenceAdenocarcinomaAnimalsBase SequenceBinding SitesCell Line, TumorCell Transformation, NeoplasticCellular SenescenceChromatin Assembly and DisassemblyCpG IslandsDNA MethylationEpigenesis, GeneticFemaleGene ExpressionGene Expression Regulation, NeoplasticGenes, Tumor SuppressorBMI1 protein, humanHepatocyte Nuclear Factor 1-alphahistone H2A.F-ZHistonesHNF1A protein, humanKRAS protein, humanMicroRNAsMIRN487 microRNA, humanMYC protein, humanNeoplasm ProteinsPolycomb Repressive Complex 1Polycomb Repressive Complex 2Proto-Oncogene ProteinsProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)ras ProteinsSmokeSUZ12 protein, humanTranscription FactorsTransforming Growth Factor beta1Wnt-5a ProteinWNT5A protein, humanWnt Proteins

Identifiers

PMID23426183
PMCPMC3582115

What OpenQuestion holds

Textmetadata
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.