Evidence map›Paper›PMID 23105099›Full record

ArticleThe Journal of biological chemistry2012

A novel role of Krüppel-like factor 8 in DNA repair in breast cancer cells.

Heng Lu, Liu Hu, Tianshu Li, Satadru Lahiri, Chao Shen, Melissa S Wason, Debarati Mukherjee, Hui Xie, Lin Yu, Jihe Zhao

Open access · hybridAbstract read
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. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Kruppel-like Factors in Skeletal Physiology and Pathologies.International journal of molecular sciences · 2022
    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
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

10 authors at 3 institutions in 1 country.

Heng LuBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, Florida 32827, USA.
Liu Hu
Tianshu Li
Satadru Lahiri
Chao Shen
Melissa S Wason
Debarati Mukherjee
Hui Xie
Lin Yu
Jihe Zhao
Florida College · USUniversity of Central Florida · USTranslational Research Institute for Metabolism and Diabetes · US

Funding

KLF8 Regulation of EMT Tumor MetastasisR01CA132977 · NCI · UNIVERSITY OF CENTRAL FLORIDA · PI ZHAO, JIHE · 2009 to 2014
$1.3M
NCI NIH HHS CA132977NCI NIH HHS R01 CA132977
6 · The paper itself

Abstract

Krüppel-like factor 8 (KLF8) regulates critical gene transcription and cellular events associated with cancer. However, the role of KLF8 in cancer remains largely unknown. Here, we report a surprisingly novel role for KLF8 in DNA repair in breast cancer cells. Comet, clonogenic, and WST-1 assays showed that KLF8 expression is required for protecting human breast cancer cells from doxorubicin-induced DNA damage and cell death. Western blotting indicated that overexpression of ectopic KLF8 attenuated the levels of the DNA damage marker γH2A.X in doxorubicin-treated PARP-1(+/+) but not PARP-1(-/-) mouse embryonic fibroblasts, whereas the PARP-1-binding-defective KLF8 mutant failed to do so. Interestingly, in response to the DNA damage, KLF8 was phosphorylated by the DNA-dependent protein kinase catalytic subunit and, subsequently, SUMOylated by SUMO E3 ligases protein inhibitors of activated STAT (PIASs), which depends upon the interaction of KLF8 with DNA-dependent protein kinase catalytic subunit, PIASs, and PARP-1 as well as their enzymatic activities. Lastly, we show evidence that KLF8 was recruited to the DNA damage site. These results suggest a novel role and mechanism for KLF8 in the regulation of DNA repair and therapeutic resistance in breast cancer cells.

Indexed as

AnimalsAntibiotics, AntineoplasticBreast NeoplasmsCell Line, TumorDNA-Activated Protein KinaseDNA RepairDoxorubicinDrug Resistance, NeoplasmEmbryo, MammalianFibroblastsHumansKruppel-Like Transcription FactorsMiceMice, KnockoutNeoplasm ProteinsPhosphorylationAntibiotics, AntineoplasticDNA-Activated Protein KinaseDoxorubicinKLF8 protein, humanKlf8 protein, mouseKruppel-Like Transcription FactorsNeoplasm ProteinsPARP1 protein, humanParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesRepressor ProteinsTranscription Factors

Identifiers

PMID23105099
PMCPMC3527957
OpenAlexW1978061587

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.