Evidence map›Paper›PMID 23880304›Full record

ArticleCarcinogenesis2013

Trichostatin-A modulates claudin-1 mRNA stability through the modulation of Hu antigen R and tristetraprolin in colon cancer cells.

Ashok Sharma, Ajaz A Bhat, Moorthy Krishnan, Amar B Singh, Punita Dhawan

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 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
2.0field-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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Identification ofMolecules (Basel, Switzerland) · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. AU-rich element-binding proteins in colorectal cancer.World journal of gastrointestinal oncology · 2019
    Review
  12. Review
  13. Roles of Tristetraprolin in Tumorigenesis.International journal of molecular sciences · 2018
    Review
  14. Article
  15. Review
  16. Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017
    Review
  17. 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

5 authors at 2 institutions in 1 country.

Ashok SharmaDepartment of Surgery, Vanderbilt University Medical Center, MCN, B-2211, Nashville, TN 37232, USA.
Ajaz A Bhat
Moorthy Krishnan
Amar B Singh
Punita Dhawan
Vanderbilt University Medical Center · USUniversity of Nebraska Medical Center · US

Funding

Role of Claudin-2 in Inflammatory Diseases and Colon CancerR01DK088902 · NIDDK · VANDERBILT UNIVERSITY · PI SINGH, AMAR B · 2011 to 2015
$1.7M
Regulation of Claudin-1 mediated Colon Tumor Progression and MetastasisR01CA124977 · NCI · VANDERBILT UNIVERSITY · PI DHAWAN, PUNITA · 2007 to 2011
$1.6M
NCI NIH HHS CA124977NCI NIH HHS R01 CA124977NIDDK NIH HHS DK088902NIDDK NIH HHS R01 DK088902
6 · The paper itself

Abstract

Expression of claudin-1, a tight junction protein, is highly upregulated in colon cancer. We have reported that claudin-1 expression in colon cancer cells is epigenetically regulated as histone deacetylase (HDAC) inhibitors decrease claudin-1 messenger RNA (mRNA) stability and thus expression. In this regard, our data suggested a role of the 3'-untranslated region (UTR) in the regulation of HDAC-dependent regulation of claudin-1 mRNA stability. In the current study, we demonstrate, based on our continued investigation, that the ELAV-like RNA-binding proteins (RBPs), human antigen R (HuR) and tristetraprolin (TTP) associate with the 3'-UTR of claudin-1 mRNA to modulate the latter's stability. Ribonomic and site-directed mutagenesis approaches were used to confirm the binding of HuR and TTP to the 3'-UTR of claudin-1. We further confirmed their roles in the stabilization of claudin-1 mRNA, under conditions of HDAC inhibition. In summary, we report that HuR and TTP are the critical regulators of the posttranscriptional regulation of claudin-1 expression in colon cancer cells. We also demonstrate that inhibition of HDACs by trichostatin treatment decreased the binding of HuR while increasing the binding of TTP to the 3'-UTR of claudin-1. Additionally, we provide data showing transcriptional regulation of claudin-1 expression, through the regulation of transcription factor Sp1. Taken together, we demonstrate epigenetic regulation of claudin-1 expression in colon cancer cells at the transcriptional and posttranscriptional levels.

Indexed as

3' Untranslated RegionsBase SequenceBlotting, WesternBreast NeoplasmsCells, CulturedChromatin ImmunoprecipitationClaudin-1Colonic NeoplasmsELAV ProteinsEpigenesis, GeneticFemaleFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansHydroxamic Acids3' Untranslated RegionsClaudin-1ELAV ProteinsHistone Deacetylase InhibitorsHydroxamic AcidsRNA, Messengertrichostatin ATristetraprolin

Identifiers

PMID23880304
PMCPMC3810835
OpenAlexW2148781510

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.