Evidence map›Paper›PMID 28650468›Full record

ArticleOncogene2017

MKP-1 suppresses PARP-1 degradation to mediate cisplatin resistance.

J Wang, D H Kho, J-Y Zhou, R J Davis, G S Wu

Abstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Dual-specificity phosphatases: therapeutic targets in cancer therapy resistance.Journal of cancer research and clinical oncology · 2022
    Review
  7. High Expression ofFrontiers in oncology · 2022
    Article
  8. Review
  9. Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Revisiting Platinum-Based Anticancer Drugs to Overcome Gliomas.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Targeted Inhibition of the Dual Specificity Phosphatases DUSP1 and DUSP6 Suppress MPNST Growth via JNK.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  18. Article
  19. 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

5 authors at 3 institutions in 1 country.

J WangMolecular Therapeutics Program, Karmanos Cancer Institute, Detroit, MI, USA.
D H KhoMolecular Therapeutics Program, Karmanos Cancer Institute, Detroit, MI, USA.
J-Y ZhouMolecular Therapeutics Program, Karmanos Cancer Institute, Detroit, MI, USA.
R J DavisProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
G S WuMolecular Therapeutics Program, Karmanos Cancer Institute, Detroit, MI, USA.
Wayne State University · USHoward Hughes Medical Institute · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
Developing targeted therapies for triple-negative breast cancerR01CA174949 · NCI · WAYNE STATE UNIVERSITY · PI WU, GEN SHENG · 2014 to 2020
$1.4M
NCI NIH HHS P30 CA022453NCI NIH HHS R01 CA174949
6 · The paper itself

Abstract

Understanding the mechanisms of platinum compound resistance, including cisplatin resistance, has important implications for improving cancer treatments. Previous studies identified a potential role for mitogen-activated protein kinase phosphatase-1 (MKP-1) in cisplatin resistance. This work focuses on the regulation of poly(ADP-ribose) polymerase-1 (PARP-1) expression by MKP-1. We found that MKP-1 overexpression stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and cisplatin resistance while its downregulation suppresses PARP-1 and PAR protein expression and cisplatin resistance. Silencing MKP-1 promoted PARP-1 ubiquitination, which decreased PARP-1 protein levels. We also found that silencing c-Jun N-terminal kinase 1/2 (JNK1/2) decreased PARP-1 ubiquitination while increasing total PARP-1 protein levels. Furthermore, we showed that acquired cisplatin-resistant ovarian cancer cells expressed high levels of MKP-1 and PARP-1 proteins, and that silencing MKP-1 or PARP-1 increased cisplatin sensitivity in resistant cells. Notably, the pharmacologic inhibition of PARP activity restored cisplatin sensitivity in MKP-1 overexpressing cells. Thus, this work indicates that suppression of JNK1/2 activity by MKP-1 maintains PARP-1 levels and suggests that MKP-1-mediated cisplatin resistance can be bypassed by PARP-1 inhibition.

Indexed as

Cell Line, TumorCisplatinDrug Resistance, NeoplasmDual Specificity Phosphatase 1FemaleGene Expression Regulation, NeoplasticGene SilencingHumansJNK Mitogen-Activated Protein KinasesOvarian NeoplasmsPoly (ADP-Ribose) Polymerase-1ProteolysisCisplatinDual Specificity Phosphatase 1DUSP1 protein, humanJNK Mitogen-Activated Protein KinasesPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1

Identifiers

PMID28650468
PMCPMC5658239
OpenAlexW2680461124

What OpenQuestion holds

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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.