Evidence map›Paper›PMID 23417858›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013

Overexpression of microRNA-21 regulating PDCD4 during tumorigenesis of liver fluke-associated cholangiocarcinoma contributes to tumor growth and metastasis.

P Chusorn, N Namwat, W Loilome, A Techasen, C Pairojkul, N Khuntikeo, A Dechakhamphu, C Talabnin, W Chan-On, C K Ong and 2 more

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Cholangiocarcinoma 2020: the next horizon in mechanisms and management.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  11. Article
  12. NcRNAs and Cholangiocarcinoma.Journal of Cancer · 2018
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Knockout of microRNA-21 reduces biliary hyperplasia and liver fibrosis in cholestatic bile duct ligated mice.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
  18. 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

12 authors at 4 institutions in 2 countries.

P ChusornDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
N Namwat
W Loilome
A Techasen
C Pairojkul
N Khuntikeo
A Dechakhamphu
C Talabnin
W Chan-On
C K Ong
B T Teh
P Yongvanit
Khon Kaen University · THNational Cancer Centre Singapore · SGSuranaree University of Technology · THUbon Ratchathani Rajabhat University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA, an endogenous noncoding RNA modulating gene expression, is a key molecule that by its dysregulation plays roles in inflammatory-driven carcinogenesis. This study aimed to investigate the role of oncomiR miR-21 and its target, the programmed cell death 4 (PDCD4) in tumor growth and metastasis of the liver fluke Opisthorchis viverrini-associated cholangiocarcinoma (CCA). The expression levels of miR-21 and PDCD4 were analyzed using the TaqMan miRNA expression assay and immunohistochemistry in liver tissues of both O. viverrini plus N-nitrosodimethylamine (NDMA)-treated hamsters and human CCA samples (n=23 cases). The functional assay for miR-21 was performed in CCA cell lines by the anti-miR-21 and pre-miR-21 transfection procedures. The peak of miR-21 levels were reached at 2 (hyperplastic lesions) and 6 (CCA) months of the O. viverrini plus NDMA-induced group and had a reverse response with its target PDCD4 proteins. In human CCA, miR-21 was overexpressed in tumor tissues when compared with nontumor tissues (P=0.0034) and had a negative correlation with PDCD4 protein (P=0.026). It was also found that high expression of miR-21 was significantly correlated with shorter survival (P<0.05) and lymph node metastasis (P=0.037) of CCA patients. Transient transfection of pre-miR-21 reduced the PDCD4 level and resulted in an increase of M213 CCA cell growth and wound-induced migration ability. These results indicated that miR-21 plays a role in the carcinogenesis and metastasis of O. viverrini-associated CCA by suppressing the function of PDCD4. Modulation of aberrantly expressed miR-21 may be a useful strategy to inhibit tumor cell phenotypes or improve response to chemotherapy.

Indexed as

Cell ProliferationAnimalsApoptosisApoptosis Regulatory ProteinsBile Duct NeoplasmsBile DuctsBile Ducts, IntrahepaticBlotting, WesternCell MovementCholangiocarcinomaCricetinaeFasciola hepaticaFascioliasisFemaleHumansImmunoenzyme TechniquesApoptosis Regulatory ProteinsMicroRNAsMIRN21 microRNA, humanPDCD4 protein, humanRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID23417858
OpenAlexW2086003545

What OpenQuestion holds

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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.