Evidence map›Paper›PMID 23461975›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2013

Silibinin synergizes with histone deacetylase and DNA methyltransferase inhibitors in upregulating E-cadherin expression together with inhibition of migration and invasion of human non-small cell lung cancer cells.

Samiha Mateen, Komal Raina, Chapla Agarwal, Daniel Chan, Rajesh Agarwal

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Milk Thistle (Current medicinal chemistry · 2025
    Review
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  12. Article
  13. Review
  14. The Emerging Roles of Heterochromatin in Cell Migration.Frontiers in cell and developmental biology · 2020
    Review
  15. Article
  16. Article
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  18. 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

5 authors at 3 institutions in 1 country.

Samiha MateenDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy, University of Colorado Anschutz Medical Campus, 12850 E. Montview Blvd, C238, Aurora, CO 80045, USA.
Komal Raina
Chapla Agarwal
Daniel Chan
Rajesh Agarwal
University of Colorado Anschutz Medical Campus · USUniversity of Montana · USUniversity of Colorado Cancer Center · US

Funding

Prostate cancer prevention and treatment by sillibininR01CA102514 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2003 to 2013
$3.6M
Angioprevention of Lung Tumorigenesis by SilibininR01CA113876 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2005 to 2009
$1.5M
NCI NIH HHS CA102514NCI NIH HHS CA113876NCI NIH HHS R01 CA102514NCI NIH HHS R01 CA113876
6 · The paper itself

Abstract

Aggressive cancers in the epithelial-to-mesenchymal transition (EMT) phase are characterized by loss of cell adhesion, repression of E-cadherin, and increased cell mobility. Non-small cell lung cancer (NSCLC) differs in basal level of E-cadherin; predominantly exhibiting silenced expression due to epigenetic-related modifications. Accordingly, effective treatments are needed to modulate these epigenetic events that in turn can positively regulate E-cadherin levels. Herein, we investigated silibinin, a natural flavonolignan with anticancer efficacy against lung cancer, either alone or in combination with epigenetic therapies to modulate E-cadherin expression in a panel of NSCLC cell lines. Silibinin combined with HDAC inhibitor Trichostatin A [TSA; 7-[4-(dimethylamino)phenyl]-N-hydroxy-4,6-dimethyl-7-oxohepta-2,4-dienamide] or DNMT inhibitor 5'-Aza-deoxycytidine (Aza) significantly restored E-cadherin levels in NSCLC cells harboring epigenetically silenced E-cadherin expression. These combination treatments also strongly decreased the invasion/migration of these cells, which further emphasized the biologic significance of E-cadherin restoration. Treatment of NSCLC cells, with basal E-cadherin levels, by silibinin further increased the E-cadherin expression and inhibited their migratory and invasive potential. Additional studies showed that silibinin alone as well as in combination with TSA or Aza downmodulate the expression of Zeb1, which is a major transcriptional repressor of E-cadherin. Overall these findings demonstrate the potential of combinatorial treatments of silibinin with HDAC or DNMT inhibitor to modulate EMT events in NSCLC cell lines, leading to a significant inhibition in their migratory and invasive potentials. These results are highly significant, since loss of E-cadherin and metastatic spread of the disease via EMT is associated with poor prognosis and high mortalities in NSCLC.

Indexed as

AntioxidantsAzacitidineBlotting, WesternCadherinsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementDecitabineDrug SynergismEnzyme InhibitorsEpigenesis, GeneticGene SilencingHistone Deacetylase InhibitorsHomeodomain ProteinsHumansHydroxamic AcidsAntioxidantsAzacitidineCadherinsDecitabineEnzyme InhibitorsHistone Deacetylase InhibitorsHomeodomain ProteinsHydroxamic AcidsSilybinSilymarinTranscription Factorstrichostatin AZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID23461975
PMCPMC3629797
OpenAlexW1999546839

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.