Evidence map›Paper›PMID 26025929›Full record

ArticleOncotarget2015

Identification of epidermal growth factor receptor and its inhibitory microRNA141 as novel targets of Krüppel-like factor 8 in breast cancer.

Tianshu Li, Heng Lu, Debarati Mukherjee, Satadru K Lahiri, Chao Shen, Lin Yu, Jihe Zhao

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Regulation of Krüppel-like factor 8 by the NEDD4 E3 ubiquitin ligase.American journal of translational research · 2019
    Article
  11. 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

7 authors at 3 institutions in 2 countries.

Tianshu LiBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
Heng LuBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
Debarati MukherjeeBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
Satadru K LahiriBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
Chao ShenBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
Lin YuBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
Jihe ZhaoBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
University of Central Florida · USFlorida College · USCleveland Clinic Lerner College of Medicine · US

Funding

KLF8 Regulation of EMT Tumor MetastasisR01CA132977 · NCI · UNIVERSITY OF CENTRAL FLORIDA · PI ZHAO, JIHE · 2009 to 2014
$1.3M
NCI NIH HHS R01 CA132977NCI NIH HHS R01CA132977
6 · The paper itself

Abstract

Krüppel-like factor 8 (KLF8) is a dual transcriptional factor critical for breast cancer progression. Epidermal growth factor receptor (EGFR) is frequently overexpressed in aggressive such as triple-negative breast cancer and associated with poor clinical outcomes. Here we report a novel KLF8-EGFR signaling axis in breast cancer. We identified a highly correlated co-overexpression between KLF8 and EGFR in invasive breast cancer cells and patient tumor samples. Overexpression of KLF8 in the non-tumorigenic MCF-10A cells induced the expression of EGFR, whereas knockdown of KLF8 from the MDA-MB-231 cells decreased it. Promoter activation and binding assays indicated that KLF8 promotes the EGFR expression by directly binding its gene promoter. We also revealed that KLF8 directly represses the promoter of miR141 and miR141 targets the 3'-untranslational region of EGFR transcript to inhibit EGFR translation. Treatment with the EGFR inhibitor AG1478 or overexpression of miR141 blocked the activity of ERK downstream of EGFR and inhibited KLF8-depndent cell invasiveness, proliferation and viability in cell culture and invasive growth and lung metastasis in nude mice. Conversely, overexpression of an inhibitory sponge of miR141 led to the opposite phenotypes. Taken together, these findings demonstrate a novel KLF8 to miR141/EGFR signaling pathway potentially crucial for breast cancer malignancy.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAnimalsBreast NeoplasmsCell Culture TechniquesCell Line, TumorCell ProliferationDisease ProgressionErbB ReceptorsFemaleHEK293 CellsHumansKruppel-Like Transcription FactorsMiceMice, NudeMicroRNAs3' Untranslated RegionsEGFR protein, humanErbB ReceptorsKLF8 protein, humanKruppel-Like Transcription FactorsMicroRNAsMIRN141 microRNA, humanRepressor Proteinsbreast cancerEGFRinvasion and metastasisKLF8microRNA141

Identifiers

PMID26025929
PMCPMC4673276
OpenAlexW1634224767

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.