Evidence map›Paper›PMID 22496917›Full record

ArticlePloS one2012

Role of miR-148a in hepatitis B associated hepatocellular carcinoma.

Ke Yuan, Zhaorui Lian, Bill Sun, Marcia M Clayton, Irene O L Ng, Mark A Feitelson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Autophagic Inhibition of Caveolin-1 by CompoundFrontiers in pharmacology · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Viral hepatitis and liver cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  18. Expression of the miR-148/152 Family in Acute Myeloid Leukemia and its Clinical Significance.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  19. Article
  20. Review
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

6 authors at 3 institutions in 3 countries.

Ke YuanDepartment of Biology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania, United States of America.
Zhaorui Lian
Bill Sun
Marcia M Clayton
Irene O L Ng
Mark A Feitelson
Temple University · USSbarro Health Research Organization · USUniversity of Hong Kong · HK

Funding

Early antibody markers of HCCR01CA111427 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 2005 to 2009
$1.4M
Beta-Catenin Signaling in HBxAg Mediated HCC.R01CA104025 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 2006 to 2010
$1.3M
NCI NIH HHS 5R01CA104025NCI NIH HHS 5R01CA111427NCI NIH HHS R01 CA104025NCI NIH HHS R01 CA111427
6 · The paper itself

Abstract

Hepatitis B virus encoded X antigen (HBx) is a trans-regulatory protein that alters the activity of selected transcription factors and cytoplasmic signal transduction pathways. HBx transcriptionally up-regulates the expression of a unique gene, URG11, which in turn transcriptionally up-regulates β-catenin, thereby contributing importantly to hepatocarcinogenesis. HBx and URG11 also alter the expression of multiple microRNAs, and by miRNA array analysis, both were shown to promote the expression of miR-148a. Elevated miR-148a was also seen in HBx positive liver samples from infected patients. To study the function of miR-148a, anti-148a was introduced into HepG2 and Hep3B cells stably expressing HBx or stably over-expressing URG11. Anti-miR-148a suppressed cell proliferation, cell cycle progression, cell migration, anchorage independent growth in soft agar and subcutaneous tumor formation in SCID mice. Introduction of anti-miR-148a increased PTEN protein and mRNA expression, suggesting that PTEN was targeted by miR-148a. Anti-miR-148a failed to suppress PTEN expression when co-transfected with reporter gene mutants in the 3'UTR of PTEN mRNA. Introduction of anti-miR-148a also resulted in depressed Akt signaling by HBx and URG11, resulting in decreased expression of β-catenin. Thus, miR-148a may play a central role in HBx/URG11 mediated HCC, and may be an early diagnostic marker and/or therapeutic target associated with this tumor type.

Indexed as

3' Untranslated RegionsAdultAgedAnimalsbeta CateninCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCell ProliferationFemaleHepatitis BHumansLiver NeoplasmsMaleMice3' Untranslated Regionsbeta CateninCTNNB1 protein, humanhepatitis B virus X proteinMicroRNAsMIRN148 microRNA, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTrans-ActivatorsViral Regulatory and Accessory ProteinsVWCE protein, human

Identifiers

PMID22496917
PMCPMC3322146
OpenAlexW2070235586

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.