Evidence map›Paper›PMID 18593903›Full record

ArticleCancer research2008

Methylation mediated silencing of MicroRNA-1 gene and its role in hepatocellular carcinogenesis.

Jharna Datta, Huban Kutay, Mohd W Nasser, Gerard J Nuovo, Bo Wang, Sarmila Majumder, Chang-Gong Liu, Stefano Volinia, Carlo M Croce, Thomas D Schmittgen and 2 more

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 230 papers.

0numbers the graph read from it
0cells of the map it votes in
230citing papers in PubMed
15.6field-weighted citation impact, top 1% 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

230 citing papers in PubMed, 435 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. MicroRNAs as Regulators of Cancer Cell Energy Metabolism.Journal of personalized medicine · 2022
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. MicroRNA-1: Diverse role of a small player in multiple cancers.Seminars in cell & developmental biology · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Jharna DattaDepartment of Molecular and Cellular Biochemistry, College of Pharmacy, and Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210, USA.
Huban Kutay
Mohd W Nasser
Gerard J Nuovo
Bo Wang
Sarmila Majumder
Chang-Gong Liu
Stefano Volinia
Carlo M Croce
Thomas D Schmittgen
Kalpana Ghoshal
Samson T Jacob
The Ohio State University · US

Funding

PathologyP01CA101956 · NCI · OHIO STATE UNIVERSITY · PI BYRD, JOHN C. · 2006 to 2010
$11.4M
MOLECULAR MECHANISMS OF DIET-INDUCED CARCINOGENESISR01CA086978 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA, JACOB, SAMSON T · 2002 to 2018
$4.9M
The Role of MicroRNA in HepatocarcinogenesisR21CA122694 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA · 2006 to 2007
$309k
NCI NIH HHS CA086978NCI NIH HHS CA122695NCI NIH HHS P01 CA101956NCI NIH HHS P01CA101956NCI NIH HHS R01 CA086978NCI NIH HHS R21 CA122694
6 · The paper itself

Abstract

MicroRNAs (miR) are a class of small ( approximately 21 nucleotide) noncoding RNAs that, in general, negatively regulate gene expression. Some miRs harboring CGIs undergo methylation-mediated silencing, a characteristic of many tumor suppressor genes. To identify such miRs in liver cancer, the miRNA expression profile was analyzed in hepatocellular carcinoma (HCC) cell lines treated with 5-azacytidine (DNA hypomethylating agent) and/or trichostatin A (histone deacetylase inhibitor). The results showed that these epigenetic drugs differentially regulate expression of a few miRs, particularly miR-1-1, in HCC cells. The CGI spanning exon 1 and intron 1 of miR-1-1 was methylated in HCC cell lines and in primary human HCCs but not in matching liver tissues. The miR-1-1 gene was hypomethylated and activated in DNMT1-/- HCT 116 cells but not in DNMT3B null cells, indicating a key role for DNMT1 in its methylation. miR-1 expression was also markedly reduced in primary human hepatocellular carcinomas compared with matching normal liver tissues. Ectopic expression of miR-1 in HCC cells inhibited cell growth and reduced replication potential and clonogenic survival. The expression of FoxP1 and MET harboring three and two miR-1 cognate sites, respectively, in their respective 3'-untranslated regions, was markedly reduced by ectopic miR-1. Up-regulation of several miR-1 targets including FoxP1, MET, and HDAC4 in primary human HCCs and down-regulation of their expression in 5-AzaC-treated HCC cells suggest their role in hepatocarcinogenesis. The inhibition of cell cycle progression and induction of apoptosis after re-expression of miR-1 are some of the mechanisms by which DNA hypomethylating agents suppress hepatocarcinoma cell growth.

Indexed as

DNA MethylationGene SilencingAntineoplastic AgentsApoptosisCarcinoma, HepatocellularCell CycleCell ProliferationCluster AnalysisCpG IslandsDisease ProgressionDNA (Cytosine-5-)-MethyltransferasesEnzyme InhibitorsGene Expression ProfilingGene Expression Regulation, NeoplasticHCT116 CellsHistone Deacetylase InhibitorsAntineoplastic AgentsDNA (Cytosine-5-)-MethyltransferasesEnzyme InhibitorsHistone Deacetylase InhibitorsMicroRNAs

Identifiers

PMID18593903
PMCPMC2562630
OpenAlexW1966749076

What OpenQuestion holds

Textmetadata
LicenceTDM
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.