Evidence map›Paper›PMID 21998631›Full record

ArticlePloS one2011

MiR-886-3p regulates cell proliferation and migration, and is dysregulated in familial non-medullary thyroid cancer.

Yin Xiong, Lisa Zhang, Alisha K Holloway, Xiaolin Wu, Ling Su, Electron Kebebew

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Non-coding 886 (Epigenetics · 2024
    Review
  3. The small noncoding RNARNA (New York, N.Y.) · 2024
    Article
  4. The small non-coding RNAbioRxiv : the preprint server for biology · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Are We Studying Non-Coding RNAs Correctly? Lessons from nc886.International journal of molecular sciences · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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 4 institutions in 1 country.

Yin XiongEndocrine Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Lisa Zhang
Alisha K Holloway
Xiaolin Wu
Ling Su
Electron Kebebew
Center for Cancer Research · USNational Cancer Institute · USScience Applications International Corporation (United States) · USUniversity of California, San Francisco · US

Funding

Genomic and genetic studies of endocrine cancersZIABC011275 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KEBEBEW, ELECTRON · 2010 to 2018
$8.2M
Clinical and genetic studies in familial nonmedullary thyroid cancer (FNMTC)ZIABC011287 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KEBEBEW, ELECTRON · 2010 to 2018
$3.4M
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundThe molecular basis and characteristics of familial non-medullary thyroid cancer are poorly understood. In this study, we performed microRNA (miRNA) profiling of familial and sporadic papillary thyroid cancer tumor samples. METHODOLOGY/PRINCIPAL

findingsGenome wide miRNA profiling of sporadic and familial papillary thyroid cancer was performed. Differentially expressed miRNAs were validated by quantitative RT-PCR. Ectopic expression of miR-886-3p in thyroid cancer lines was performed to identify pathways targeted by the miRNA, as well as, to determine its effect on tumor cell biology. We found four differentially expressed miRNAs between familial and sporadic papillary thyroid cancer tumor samples. MiR-886-3p and miR-20a were validated to be differentially expressed by 3- and 4-fold, respectively. Pathway analysis of genome-wide expression data on cells overexpressing miR-886-3p and target prediction analysis showed genes involved in DNA replication and focal adhesion pathways were regulated by miR-886-3p. Overexpression of miR-886-3p in thyroid cancer cell lines significantly inhibited cellular proliferation, the number and size of spheroids and cellular migration. Additionally, overexpression of miR-886-3p increased the number of cells in S phase. CONCLUSIONS/SIGNIFICANCE: Our findings for the first time suggest that miR-886-3p plays an important role in thyroid cancer tumor cell biology and regulates genes involved in DNA replication and focal adhesion. Thus, miR-886-3p may play a role in the initiation and or progression of papillary thyroid cancer.

Indexed as

Base SequenceCarcinomaCarcinoma, MedullaryCarcinoma, PapillaryCell CycleCell Line, TumorCell MovementCell ProliferationDNA ReplicationDown-RegulationFemaleFocal AdhesionsGene Expression ProfilingGenomicsHumansMaleMicroRNAsMIRN886 microRNA, humanRNA Precursors

Identifiers

PMID21998631
PMCPMC3187745
OpenAlexW2003857122

What OpenQuestion holds

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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.