Evidence map›Paper›PMID 26701725›Full record

ArticleOncotarget2016

ERK3 regulates TDP2-mediated DNA damage response and chemoresistance in lung cancer cells.

Ka Bian, Naveen Reddy Muppani, Lobna Elkhadragy, Wei Wang, Cheng Zhang, Tenghui Chen, Sungyun Jung, Ole Morten Seternes, Weiwen Long

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Atypical MAPKs in cancer.The FEBS journal · 2025
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  10. Review
  11. Molecular mechanisms of topoisomerase 2 DNA-protein crosslink resolution.Cellular and molecular life sciences : CMLS · 2020
    Review
  12. A RadioactiveBio-protocol · 2019
    Article
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  14. Review
  15. Article
  16. Article
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  19. Review
  20. Article
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

9 authors at 5 institutions in 3 countries.

Ka BianDepartment of Otorhinolaryngology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
Naveen Reddy MuppaniDepartment of Biochemistry and Molecular Biology, Wright State University, Dayton, OH, USA.
Lobna ElkhadragyDepartment of Biochemistry and Molecular Biology, Wright State University, Dayton, OH, USA.
Wei WangDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Cheng ZhangDepartment of Biochemistry and Molecular Biology, Wright State University, Dayton, OH, USA.
Tenghui ChenDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Sungyun JungDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Ole Morten SeternesDepartment of Pharmacy, University of Tromsoe, N-Tromsoe, Norway.
Weiwen LongDepartment of Biochemistry and Molecular Biology, Wright State University, Dayton, OH, USA.
Wright State University · USAir Force Medical University · CNBaylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · USUiT The Arctic University of Norway · NO

Funding

ERK3 Kinase Signaling in Lung CancerR01CA193264 · NCI · WRIGHT STATE UNIVERSITY · PI LONG, WEIWEN · 2015 to 2019
$1.7M
NCI NIH HHS 1R01CA193264-01NCI NIH HHS R01 CA193264
6 · The paper itself

Abstract

Posttranslational modifications (PTMs), such as phosphorylation and ubiquitination, play critical regulatory roles in the assembly of DNA damage response proteins on the DNA damage site and their activities in DNA damage repair. Tyrosyl DNA phosphodiesterase 2 (TDP2) repairs Topoisomerase 2 (Top2)-linked DNA damage, thereby protecting cancer cells against Top2 inhibitors-induced growth inhibition and cell death. The regulation of TDP2 activity by post-translational modifications in DNA repair, however, remains unclear. In the current study, we have found that ERK3, an atypical MAPK, phosphorylates TDP2 at S60 and regulates TDP2's phosphodiesterase activity, thereby cooperatively protecting lung cancer cells against Top2 inhibitors-induced DNA damage and growth inhibition. As such, our study revealed a post-translational regulation of TDP2 activity and discovered a new role of ERK3 in increasing cancer cells' DNA damage response and chemoresistance to Top2 inhibitors.

Indexed as

DNA DamageAnimalsAntigens, NeoplasmCell Line, TumorDNA-Binding ProteinsDNA Topoisomerases, Type IIDrug Resistance, NeoplasmEtoposideHEK293 CellsHumansLung NeoplasmsMitogen-Activated Protein Kinase 6Nuclear ProteinsPhosphoric Diester HydrolasesPhosphorylationPoly-ADP-Ribose Binding ProteinsAntigens, NeoplasmDNA-Binding ProteinsDNA Topoisomerases, Type IIEtoposideMitogen-Activated Protein Kinase 6Nuclear ProteinsPhosphoric Diester HydrolasesPoly-ADP-Ribose Binding ProteinsTDP2 protein, humanTOP2A protein, humanTopoisomerase II InhibitorsTranscription FactorschemoresistanceDNA damageERK3TDP2Top2 inhibitors

Identifiers

PMID26701725
PMCPMC4872741
OpenAlexW2274288581

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.