Evidence map›Paper›PMID 23246965›Full record

ArticleOncogene2014

ΔNp63α regulates Erk signaling via MKP3 to inhibit cancer metastasis.

J Bergholz, Y Zhang, J Wu, L Meng, E M Walsh, A Rai, M Y Sherman, Z-X Jim Xiao

Abstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

35 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  14. Transcriptional suppression of AMPKα1 promotes breast cancer metastasis upon oncogene activation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. p63 at the Crossroads between Stemness and Metastasis in Breast Cancer.International journal of molecular sciences · 2019
    Review
  19. Article
  20. Review
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 3 institutions in 2 countries.

J Bergholz1] Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA [2] Center of Growth, Metabolism and Aging, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Y ZhangCenter of Growth, Metabolism and Aging, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
J WuDepartment of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
L MengDepartment of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
E M WalshDepartment of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
A RaiDepartment of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
M Y ShermanDepartment of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
Z-X Jim Xiao1] Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA [2] Center of Growth, Metabolism and Aging, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Boston University · USSichuan University · CNState Key Laboratory of Biotherapy

Funding

XI INTERNATIONAL SYMPOSIUM ON AMYLOIDOSISP41RR010888 · NCRR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ZAIA, JOSEPH · 1996 to 2011
$18.6M
Role of MDM2 in Cell Proliferation and TumorigenesisR01CA079804 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI XIAO, ZHI-XIONG JIM · 1999 to 2010
$2.2M
Regulation of p53 in response to genotoxic stressR01GM070017 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI XIAO, ZHI-XIONG JIM · 2003 to 2006
$1.2M
NCI NIH HHS CA79804NCI NIH HHS R01 CA079804NCRR NIH HHS P41 RR010888NIGMS NIH HHS GM70017NIGMS NIH HHS R01 GM070017
6 · The paper itself

Abstract

Reduced expression of the p53 family member p63 has been suggested to play a causative role in cancer metastasis. Here, we show that ΔNp63α, the predominant p63 isoform, plays a major role in regulation of cell migration, invasion and cancer metastasis. We identified mitogen-activated protein (MAP) kinase phosphatase 3 (MKP3) as a downstream target of ΔNp63α that is required for mediating these effects. We show that ΔNp63α regulates extracellular signal-regulated protein kinases 1 and 2 (Erk1/2) activity via MKP3 in both cancer and non-transformed cells. We further show that exogenous ΔNp63α inhibits cell invasion and is dependent on MKP3 upregulation for repression. Conversely, endogenous pan-p63 ablation results in increased cell migration and invasion, which can be reverted by reintroducing the ΔNp63α isoform alone, but not by other isoforms. Interestingly, these effects require Erk2, but not Erk1 expression, and can be rescued by enforced MKP3 expression. Moreover, MKP3 expression is reduced in invasive cancers, and reduced p63 expression increases metastatic frequency in vivo. Taken together, these results suggest an important role for ΔNp63α in preventing cancer metastasis by inhibition of Erk2 signaling via MKP3.

Indexed as

AnimalsCell Line, TumorCell MovementDual Specificity Phosphatase 6Extracellular Signal-Regulated MAP KinasesFemaleHumansMAP Kinase Signaling SystemMiceNeoplasm InvasivenessNeoplasm MetastasisTranscription FactorsTumor Suppressor ProteinsDual Specificity Phosphatase 6DUSP6 protein, humanExtracellular Signal-Regulated MAP KinasesTP63 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID23246965
PMCPMC3962654
OpenAlexW1990274435

What OpenQuestion holds

Textmetadata
LicenceTDM
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.