Evidence map›Paper›PMID 24373626›Full record

ArticleMolecular cancer2013

Epigenetic inactivation of miR-9 family microRNAs in chronic lymphocytic leukemia--implications on constitutive activation of NFκB pathway.

Lu Qian Wang, Yok Lam Kwong, Chi Shan Bonnie Kho, Kit Fai Wong, Kwan Yeung Wong, Manuela Ferracin, George A Calin, Chor Sang Chim

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. miRNAs in Lymphocytic Leukaemias-The miRror of Drug Resistance.International journal of molecular sciences · 2022
    Review
  7. Regulatory role of miRNAs in Wnt signaling pathway linked with cardiovascular diseases.Current research in pharmacology and drug discovery · 2022
    Article
  8. Crosstalk Between Inflammatory Signaling and Methylation in Cancer.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Epigenetic silencing of long non-coding RNACancer cell international · 2020
    Article
  15. Article
  16. Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Review
  19. Article
  20. Epigenetic silencing of LPP/miR-28 in multiple myeloma.Journal of clinical pathology · 2018
    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

8 authors at 6 institutions in 4 countries.

Lu Qian Wang
Yok Lam Kwong
Chi Shan Bonnie Kho
Kit Fai Wong
Kwan Yeung Wong
Manuela Ferracin
George A Calin
Chor Sang ChimDepartment of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China. jcschim@hku.hk.
Queen Mary Hospital · CNUniversity of Hong Kong · HKPamela Youde Nethersole Eastern Hospital · CNQueen Elizabeth Hospital · CNThe University of Texas MD Anderson Cancer Center · USUniversity of Ferrara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe miR-9 family microRNAs have been identified as a tumor suppressor miRNA in cancers. We postulated that miR-9-1, miR-9-2 and miR-9-3 might be inactivated by DNA hypermethylation in chronic lymphocytic leukemia (CLL).

methodsMethylation of miR-9-1, miR-9-2 and miR-9-3 was studied in eight normal controls including normal bone marrow, buffy coat, and CD19-sorted peripheral blood B-cells from healthy individuals, seven CLL cell lines, and seventy-eight diagnostic CLL samples by methylation-specific polymerase chain reaction.

resultsThe promoters of miR-9-3 and miR-9-1 were both unmethylated in normal controls, but methylated in five (71.4%) and one of seven CLL cell lines respectively. However, miR-9-2 promoter was methylated in normal controls including CD19 + ve B-cells, hence suggestive of a tissue-specific but not tumor-specific methylation, and thus not further studied. Different MSP statuses of miR-9-3, including complete methylation, partial methylation, and complete unmethylation, were verified by quantitative bisulfite methylation analysis. 5-Aza-2'-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3. Moreover, overexpression of miR-9 led to suppressed cell proliferation and enhanced apoptosis together with downregulation of NFκB1 in I83-E95 cells, supporting a tumor suppressor role of miR-9-3 in CLL. In primary CLL samples, miR-9-3 was detected in 17% and miR-9-1 methylation in none of the patients at diagnosis. Moreover, miR-9-3 methylation was associated with advanced Rai stage (≥ stage 2) (P = 0.04).

conclusionsOf the miR-9 family, miR-9-3 is a tumor suppressor miRNA relatively frequently methylated, and hence silenced in CLL; whereas miR-9-1 methylation is rare in CLL. The role of miR-9-3 methylation in the constitutive activation of NFκB signaling pathway in CLL warrants further study.

Indexed as

Signal TransductionAdultAgedAged, 80 and overApoptosisCell Line, TumorCell ProliferationDNA MethylationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansLeukemia, Lymphocytic, Chronic, B-CellMaleMicroRNAsMiddle AgedMicroRNAsMIRN92 microRNA, humanNF-kappa B

Identifiers

PMID24373626
PMCPMC3877874
OpenAlexW2138781403

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LicenceCC BY
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Registered trials

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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.