Evidence map›Paper›PMID 23678002›Full record

ArticleThe Journal of biological chemistry2013

Differential regulation of c-Jun protein plays an instrumental role in chemoresistance of cancer cells.

Yan Xia, Weiwei Yang, Wen Bu, Haitao Ji, Xueqiang Zhao, Yanhua Zheng, Xin Lin, Yi Li, Zhimin Lu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. p21Cancers · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Advances in delivery systems for doxorubicin.Journal of nanomedicine & nanotechnology · 2018
    Article
  10. Article
  11. Review
  12. Review
  13. 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

9 authors at 3 institutions in 2 countries.

Yan XiaBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Weiwei Yang
Wen Bu
Haitao Ji
Xueqiang Zhao
Yanhua Zheng
Xin Lin
Yi Li
Zhimin Lu
Pediatric Brain Tumor Foundation · USThe University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
The Role of b-catenin in EGFR-Related Tumor DevelopmentR01CA109035 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, ZHIMIN · 2005 to 2016
$2.7M
The Mechanisms of PKM2-Regulated Gene Expression in Tumor Development.R01CA169603 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, ZHIMIN · 2013 to 2017
$1.7M
Oncogene susceptibility: physiological state & breast cell differentiationR01CA124820 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LI, YI · 2010 to 2014
$1.5M
NCI NIH HHS 1R01 CA169603NCI NIH HHS 2R01 CA109035NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA109035NCI NIH HHS R01 CA124820NCI NIH HHS R01 CA169603
6 · The paper itself

Abstract

The chemotherapeutic drug cisplatin (cis-diamminedichloroplatinum(II) (CDDP)) is widely used in the treatment of human cancers. However, the mechanism underlying intrinsic tumor resistance to CDDP remains elusive. Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9-dependent cleavage of c-Jun at Asp-65 and MEKK1-mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells. In contrast, activation of JNK2 (but not JNK1) phosphorylated and up-regulated the expression of c-Jun in CDDP-resistant cells. Activated c-Jun bound to the promoter regions of the MDR1 gene and promoted the expression of MDR1. Expression of a cleavage-resistant c-Jun mutant (D65A) suppressed CDDP-induced apoptosis of CDDP-sensitive cells, whereas depletion of JNK2, c-Jun, or MDR1 in CDDP-resistant cancer cells promoted apoptosis upon CDDP treatment. In addition, mammary gland tumors induced by polyomavirus middle T antigen in JNK2(-/-) mice were more sensitive to CDDP compared with those in JNK2(+/+) mice. These findings highlight the instrumental role of c-Jun in the resistance of tumors to treatment with CDDP and indicate that c-Jun is a molecular target for improving cancer therapy.

Indexed as

AnimalsAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1Caspase 9Cell Line, TumorCisplatinDrug Resistance, NeoplasmFemaleHumansMammary Neoplasms, AnimalMAP Kinase Kinase Kinase 1MiceMice, KnockoutMitogen-Activated Protein Kinase 9Proto-Oncogene Proteins c-junUbiquitinationAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1Casp9 protein, mouseCaspase 9CisplatinMAP Kinase Kinase Kinase 1Mitogen-Activated Protein Kinase 9Proto-Oncogene Proteins c-junApoptosisCaspasec-Junc-Jun N-terminal Kinase (JNK)Jun Transcription FactorUbiquitin

Identifiers

PMID23678002
PMCPMC3707636
OpenAlexW2001281846

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.