Evidence map›Paper›PMID 22438909›Full record

ArticlePloS one2012

Blimp1 activation by AP-1 in human lung cancer cells promotes a migratory phenotype and is inhibited by the lysyl oxidase propeptide.

Ziyang Yu, Seiichi Sato, Philip C Trackman, Kathrin H Kirsch, Gail E Sonenshein

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Blimp-1 Upregulation by Multiple LigandsFrontiers in pharmacology · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. TF/FVIIa/PAR2 promotes cell proliferation and migration via PKCα and ERK-dependent c-Jun/AP-1 pathway in colon cancer cell line SW620.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  17. 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 2 institutions in 1 country.

Ziyang YuDepartment of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Seiichi Sato
Philip C Trackman
Kathrin H Kirsch
Gail E Sonenshein
Tufts University · USBoston University · US

Funding

Signaling Pathways in Stages of TumorigenesisP01ES011624 · NIEHS · TUFTS UNIVERSITY BOSTON · PI SONENSHEIN, GAIL E. · 2001 to 2012
$11.4M
Lysyl Oxidase Propeptide: Breast Cancer InhibitorR01CA143108 · NCI · TUFTS UNIVERSITY BOSTON · PI SONENSHEIN, GAIL E. · 2010 to 2014
$2.5M
NCI NIH HHS R01 CA143108NIEHS NIH HHS P01 ES011624
6 · The paper itself

Abstract

B lymphocyte-induced maturation protein 1 (Blimp1) is a master regulator of B cell differentiation, and controls migration of primordial germ cells. Recently we observed aberrant Blimp1 expression in breast cancer cells resulting from an NF-κB RelB to Ras signaling pathway. In order to address the question of whether the unexpected expression of Blimp1 is seen in other epithelial-derived tumors, we selected lung cancers as they are frequently driven by Ras signaling. Blimp1 was detected in all five lung cancer cell lines examined and shown to promote lung cancer cell migration and invasion. Interrogation of microarray datasets demonstrated elevated BLIMP1 RNA expression in lung adenocarcinoma, pancreatic ductal carcinomas, head and neck tumors as well as in glioblastomas. Involvement of Ras and its downstream kinase c-Raf was confirmed using mutant and siRNA strategies. We next addressed the issue of mechanism of Blimp1 activation in lung cancer. Using knockdown and ectopic expression, the role of the Activator Protein (AP)-1 family of transcription factors was demonstrated. Further, chromatin immunoprecipitation assays confirmed binding to identified AP-1 elements in the BLIMP1 promoter of ectopically expressed c-Jun and of endogenous AP-1 subunits following serum stimulation. The propeptide domain of lysyl oxidase (LOX-PP) was identified as a tumor suppressor, with ability to reduce Ras signaling in lung cancer cells. LOX-PP reduced expression of Blimp1 by binding to c-Raf and inhibiting activation of AP-1, thereby attenuating the migratory phenotype of lung cancer cells. Thus, Blimp1 is a mediator of Ras/Raf/AP-1 signaling that promotes cell migration, and is repressed by LOX-PP in lung cancer.

Indexed as

AnimalsBase SequenceCell Line, TumorCell MovementDNA PrimersHumansJNK Mitogen-Activated Protein KinasesLung NeoplasmsMicePhenotypePositive Regulatory Domain I-Binding Factor 1Promoter Regions, GeneticProtein-Lysine 6-OxidaseProtein Structure, TertiaryProto-Oncogene Proteins c-rafras ProteinsDNA PrimersJNK Mitogen-Activated Protein KinasesPositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanProtein-Lysine 6-OxidaseProto-Oncogene Proteins c-rafras ProteinsRecombinant ProteinsRepressor ProteinsRNA, NeoplasmTranscription Factor AP-1

Identifiers

PMID22438909
PMCPMC3305320
OpenAlexW2013866007

What OpenQuestion holds

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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.