Evidence map›Paper›PMID 22547075›Full record

ArticleThe Journal of biological chemistry2012

DNA damage induces NF-κB-dependent microRNA-21 up-regulation and promotes breast cancer cell invasion.

Jixiao Niu, Yuling Shi, Guangyun Tan, Chuan He Yang, Meiyun Fan, Lawrence M Pfeffer, Zhao-Hui Wu

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
7.4field-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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Review
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  12. Review
  13. Review
  14. MicroRNA Networks Modulate Oxidative Stress in Cancer.International journal of molecular sciences · 2019
    Review
  15. Article
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  17. Review
  18. Review
  19. Article
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 2 countries.

Jixiao NiuDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38103, USA.
Yuling Shi
Guangyun Tan
Chuan He Yang
Meiyun Fan
Lawrence M Pfeffer
Zhao-Hui Wu
University of Tennessee Health Science Center · US

Funding

Strategies to improve the antiglioma action of IFN-?: a role for NF-kB inhibitionR01CA133322 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI DAVIDOFF, ANDREW M, PFEFFER, LAWRENCE MARC · 2009 to 2013
$2.6M
Genotoxic NF-kB Signaling in CancerR01CA149251 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WU, ZHAOHUI · 2011 to 2015
$1.5M
Molecular mechanism of ID1 function in advanced breast cancerR01CA140346 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI FAN, MEIYUN · 2009 to 2013
$1.2M
NCI NIH HHS CA133322NCI NIH HHS CA149251NCI NIH HHS R01 CA133322NCI NIH HHS R01 CA140346NCI NIH HHS R01 CA149251
6 · The paper itself

Abstract

NF-κB activation induced by genotoxic treatment in cancer cells has been associated with therapeutic resistance in multiple human malignancies. Therapeutic resistance also correlates with high metastatic potential in human cancers, including breast cancer. Whether genotoxic treatment-activated NF-κB also contributes to cancer metastasis following radiation and chemotherapy is unclear. Here, we show that chemotherapeutic drug-induced NF-κB activation promotes breast cancer cell migration and invasion. The increased metastatic potential is dependent on IL-6 induction mediated by genotoxic NF-κB activation. Moreover, genotoxic treatment also up-regulates oncogenic microRNA-21 (miR-21) expression through eliciting NF-κB recruitment to the miR-21 promoter region, where it cooperates with signal transducer and activator of transcription 3 (STAT3) to activate miR-21 transcription. DNA damage-induced histone H3 phosphorylation via activated MSK1 creates an open chromatin structure for NF-κB/STAT3-driven transactivation of miR-21. NF-κB-dependent IL-6 up-regulation is responsible for STAT3 activation and recruitment to the miR-21 promoter upon genotoxic stress. Induction of miR-21 may enable cancer cells to elude DNA damage-induced apoptosis and enhance the metastatic potential of breast cancer cells through repressing expression of PTEN and PDCD4. Our data support a critical role of DNA damage-induced NF-κB activation in promoting cancer metastasis following genotoxic treatment, and NF-κB-dependent miR-21 induction may contribute to both therapeutic resistance and metastasis in breast cancer.

Indexed as

DNA DamageAnimalsBreast NeoplasmsCell LineCell Line, TumorCell SurvivalEnzyme-Linked Immunosorbent AssayFibroblastsGene Expression Regulation, NeoplasticHumansInterleukin-6MiceMicroRNAsMutagensNeoplasm MetastasisNF-kappa BInterleukin-6MicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mouseMutagensNF-kappa BSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID22547075
PMCPMC3381141
OpenAlexW2029194329

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.