Evidence map›Paper›PMID 21706057›Full record

ArticleOncogene2012

Identification of a c-Jun N-terminal kinase-2-dependent signal amplification cascade that regulates c-Myc levels in ras transformation.

D P Mathiasen, C Egebjerg, S H Andersen, B Rafn, P Puustinen, A Khanna, M Daugaard, E Valo, S Tuomela, T Bøttzauw and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

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  6. CIP2A silencing alleviates doxorubicin resistance in MCF7/ADR cells through activating PP2A and autophagy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
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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

17 authors at 7 institutions in 2 countries.

D P MathiasenApoptosis Department and Centre for Genotoxic Stress Research, Institute of Cancer Biology, Danish Cancer Society, Copenhagen, Denmark.
C Egebjerg
S H Andersen
B Rafn
P Puustinen
A Khanna
M Daugaard
E Valo
S Tuomela
T Bøttzauw
C F Nielsen
B M Willumsen
S Hautaniemi
R Lahesmaa
J Westermarck
M Jäättelä
T Kallunki
Danish Cancer Society · DKUniversity of Helsinki · FIÅbo Akademi University · FITampere University of Applied Sciences · FITurku Centre for Biotechnology · FIUniversity of Copenhagen · DKUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras is one of the most frequently activated oncogenes in cancer. Two mitogen-activated protein kinases (MAPKs) are important for ras transformation: extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase 2 (JNK2). Here we present a downstream signal amplification cascade that is critical for ras transformation in murine embryonic fibroblasts. This cascade is coordinated by ERK and JNK2 MAPKs, whose Ras-mediated activation leads to the enhanced levels of three oncogenic transcription factors, namely, c-Myc, activating transcription factor 2 (ATF2) and ATF3, all of which are essential for ras transformation. Previous studies show that ERK-mediated serine 62 phosphorylation protects c-Myc from proteasomal degradation. ERK is, however, not alone sufficient to stabilize c-Myc but requires the cooperation of cancerous inhibitor of protein phosphatase 2A (CIP2A), an oncogene that counteracts protein phosphatase 2A-mediated dephosphorylation of c-Myc. Here we show that JNK2 regulates Cip2a transcription via ATF2. ATF2 and c-Myc cooperate to activate the transcription of ATF3. Remarkably, not only ectopic JNK2, but also ectopic ATF2, CIP2A, c-Myc and ATF3 are sufficient to rescue the defective ras transformation of JNK2-deficient cells. Thus, these data identify the key signal converging point of JNK2 and ERK pathways and underline the central role of CIP2A in ras transformation.

Indexed as

MAP Kinase Signaling SystemActivating Transcription Factor 2Activating Transcription Factor 3AnimalsCells, CulturedCell Transformation, NeoplasticFibroblastsGenes, rasMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase 9Protein Phosphatase 2Proto-Oncogene Proteins c-mycras ProteinsActivating Transcription Factor 2Activating Transcription Factor 3Atf2 protein, mouseAtf3 protein, mouseMitogen-Activated Protein Kinase 9Myc protein, mouseProtein Phosphatase 2Proto-Oncogene Proteins c-mycras Proteins

Identifiers

PMID21706057
OpenAlexW2067854511

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.