Evidence map›Paper›PMID 20356845›Full record

ArticleThe Journal of biological chemistry2010

Kruppel-like factor 4 inhibits epithelial-to-mesenchymal transition through regulation of E-cadherin gene expression.

Jennifer L Yori, Emhonta Johnson, Guangjin Zhou, Mukesh K Jain, Ruth A Keri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 2 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Review
  7. Cells · 2025
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  10. Synergistic effects of combined cisplatin andJournal of Taibah University Medical Sciences · 2023
    Article
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  12. Review
  13. Article
  14. Frontiers in immunology · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. SIRT2-KLF4 Interactions are Critical for Myeloma Survival and Migration.Computational intelligence and neuroscience · 2022
    Article
  20. Article

50 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

5 authors at 2 institutions in 1 country.

Jennifer L YoriDepartment of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Emhonta Johnson
Guangjin Zhou
Mukesh K Jain
Ruth A Keri
University Hospitals Case Medical Center · USCase Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
KLF2, monocyte activation and vascular inflammationR01HL086548 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2007 to 2016
$3.5M
Regulation of erbB2/Neu-induced mammary gland cancerR01CA090398 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI KERI, RUTH A. · 2001 to 2011
$2.7M
KLF4, Monocyte Biology and Vasculary InjuryR01HL075427 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2004 to 2010
$2.6M
NCI NIH HHS CA090398NCI NIH HHS P30 CA043703NCI NIH HHS R01 CA090398NHLBI NIH HHS HL075427NHLBI NIH HHS HL086548NHLBI NIH HHS R01 HL075427NHLBI NIH HHS R01 HL086548
6 · The paper itself

Abstract

The Krüppel-like factor 4 (KLF4) is a transcriptional regulator of proliferation and differentiation in epithelial cells, both during development and tumorigenesis. Although KLF4 functions as a tumor suppressor in several tissues, including the colon, the role of KLF4 in breast cancer is less clear. Here, we show that KLF4 is necessary for maintenance of the epithelial phenotype in non-transformed MCF-10A mammary epithelial cells. KLF4 silencing led to alterations in epithelial cell morphology and migration, indicative of an epithelial-to-mesenchymal transition. Consistent with these changes, decreased levels of KLF4 also resulted in the loss of E-cadherin protein and mRNA. Promoter/reporter analyses revealed decreased E-cadherin promoter activity with KLF4 silencing, while chromatin immunoprecipitation identified endogenous KLF4 binding to the GC-rich/E-box region of this promoter. Furthermore, forced expression of KLF4 in the highly metastatic MDA-MB-231 breast tumor cell line was sufficient to restore E-cadherin expression and suppress migration and invasion. These findings identify E-cadherin as a novel transcriptional target of KLF4. The clear requirement for KLF4 to maintain E-cadherin expression and prevent epithelial-to-mesenchymal transition in mammary epithelial cells supports a metastasis suppressive role for KLF4 in breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBreast NeoplasmsCadherinsCell Line, TumorCell MovementCell ProliferationEpitheliumHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMesodermModels, BiologicalNeoplasm MetastasisPromoter Regions, GeneticRNA, MessengerCadherinsKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsRNA, Messenger

Identifiers

PMID20356845
PMCPMC2878056
OpenAlexW2044224053

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.