Evidence map›Paper›PMID 24675421›Full record

ArticleOncotarget2014

Retaining MKP1 expression and attenuating JNK-mediated apoptosis by RIP1 for cisplatin resistance through miR-940 inhibition.

Qiong Wang, Shaoqing Shi, Weiyang He, Mabel T Padilla, Lin Zhang, Xia Wang, Bin Zhang, Yong Lin

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

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Dual-specificity phosphatases: therapeutic targets in cancer therapy resistance.Journal of cancer research and clinical oncology · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. RIPK1 binds to vitamin D receptor and decreases vitamin D-induced growth suppression.The Journal of steroid biochemistry and molecular biology · 2017
    Article
  18. Review
  19. Article
  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

8 authors at 4 institutions in 2 countries.

Qiong WangLaboratory of Molecular and Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education at Sichuan University, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, P.R. China.
Shaoqing Shi
Weiyang He
Mabel T Padilla
Lin Zhang
Xia Wang
Bin Zhang
Yong Lin
Lovelace Respiratory Research Institute · USSichuan University · CNChongqing Medical University · CNChongqing Public Health Medical Center · CN

Funding

Bridging Inflammation and Cigarette Smoke-associated Lung Carcinogenesis by MUC1R01ES017328 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2010 to 2014
$2.2M
NIEHS NIH HHS R01 ES017328NIEHS NIH HHS R01ES017328
6 · The paper itself

Abstract

The elucidation of chemoresistance mechanisms is important to improve cancer patient survival. In this report, we investigated the role and mechanism through which receptor-interacting protein 1 (RIP1), a mediator in cell survival and death signaling, participates in cancer's response to chemotherapy. In lung cancer cells, knockdown of RIP1 substantially increased cisplatin-induced apoptotic cytotoxicity, which was associated with robust JNK activation. The expression of the JNK inactivating phosphatase, MKP1, was substantially reduced in RIP1 knockdown cells. Although MKP1 protein stability was not altered by RIP1 suppression, the synthesis rate of MKP1 was dramatically reduced in RIP1-suppressed cells. Furthermore, we found that the expression of miR-940 was substantially increased in RIP1 knockdown cells. Knockdown of miR-940 restored MKP1 expression and attenuated cisplatin-induced JNK activation and cytotoxicity. Importantly, ectopic expression of MKP1 effectively attenuated cisplatin-induced JNK activation and cytotoxicity. In addition, activation of the JNK upstream signaling kinase, MKK4, was also potentiated in RIP1 knockdown cells. Altogether, our results suggest that RIP1 contributes to cisplatin resistance by suppressing JNK activation that involves releasing miR-940-mediated inhibition of MKP1 and suppressing activation of MKK4. Intervention targeting the RIP1/miR-940/MKP1/JNK pathway may be used to sensitize platinum-based chemotherapy.

Indexed as

Antineoplastic AgentsApoptosisCell Line, TumorCisplatinDrug Resistance, NeoplasmDual Specificity Phosphatase 1Gene ExpressionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4MicroRNAsNuclear Pore Complex ProteinsRNA-Binding ProteinsRNA, MessengerAGFG1 protein, humanAntineoplastic AgentsCisplatinDual Specificity Phosphatase 1DUSP1 protein, humanJNK Mitogen-Activated Protein KinasesMAP2K4 protein, humanMAP Kinase Kinase 4MicroRNAsMIRN940 microRNA, humanNuclear Pore Complex ProteinsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID24675421
PMCPMC4012727
OpenAlexW2106880246

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.