Evidence map›Paper›PMID 21518959›Full record

ArticleMolecular and cellular biology2011

A KLF4-miRNA-206 autoregulatory feedback loop can promote or inhibit protein translation depending upon cell context.

Chen-Chung Lin, Ling-Zhi Liu, Joseph B Addison, William F Wonderlin, Alexey V Ivanov, J Michael Ruppert

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.0field-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

70 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  5. Human keratinocyte response to 4,4'-methylene diphenyl diisocyanate-glutathione conjugate exposure.Xenobiotica; the fate of foreign compounds in biological systems · 2024
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  6. Review
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Extracellular MicroRNA-92a Mediates Endothelial Cell-Macrophage Communication.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  19. Identification of two microRNA nodes as potential cooperative modulators of liver metabolism.Hepatology research : the official journal of the Japan Society of Hepatology · 2019
    Article
  20. Article

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

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 1 institution in 1 country.

Chen-Chung LinDepartment of Biochemistry, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Ling-Zhi Liu
Joseph B Addison
William F Wonderlin
Alexey V Ivanov
J Michael Ruppert
West Virginia University · US

Funding

THE ROLE OF HEF1 PROTEIN IN INVASION OF METASTATIC BREAST CANCERP20RR016440 · NCRR · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2001 to 2010
$22.8M
Klf4 in tumor initiation and maintenance of squamous cell carcinomaR01CA127405 · NCI · WEST VIRGINIA UNIVERSITY · PI RUPPERT, JOHN MICHAEL · 2007 to 2011
$1.4M
NCI NIH HHS R01 CA127405NCRR NIH HHS P20 RR016440NCRR NIH HHS RR 016440
6 · The paper itself

Abstract

Krüppel-like factor 4 (KLF4), a transcription factor that regulates cell fate in a context-dependent fashion, is normally induced upon growth arrest or differentiation. In many cancer cells there is dysregulation, with increased expression in proliferating cells. To identify sequence elements that mediate KLF4 suppression in normal epithelial cells, we utilized a luciferase reporter and RK3E cells, which undergo a proliferation-differentiation switch to form an epithelial sheet. A translational control element (TCE) within the KLF4 3'-untranslated region interacted with microRNAs (miRs) 206 and 344-1 to promote or inhibit KLF4 expression, respectively, in proliferating epithelial cells. Overall, the TCE suppressed expression in proliferating primary human mammary epithelial cells, but this suppressive effect was attenuated in immortalized mammary epithelial MCF10A cells, in which Dicer1 and miR-206 promoted KLF4 expression and TCE reporter activity. In contrast to MCF10A cells, in breast cancer cells the activity of miR-206 was switched, and it repressed KLF4 expression and TCE reporter activity. As miR-206 levels were KLF4 dependent, the results identify a KLF4-miR-206 feedback pathway that oppositely affects protein translation in normal cells and cancer cells. In addition, the results indicate that two distinct miRs can have opposite and competing effects on translation in proliferating cells.

Indexed as

Protein BiosynthesisAnimalsBase SequenceCell CycleCell DifferentiationCell LineCell ProliferationEpithelial CellsFeedback, PhysiologicalHomeostasisHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMammary Glands, HumanMicroRNAsMolecular Sequence DataKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN206 microRNA, human

Identifiers

PMID21518959
PMCPMC3133414
OpenAlexW2147295142

What OpenQuestion holds

Textmetadata
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.