Evidence map›Paper›PMID 26411364›Full record

ArticleOncogene2016

CPEB1 mediates epithelial-to-mesenchyme transition and breast cancer metastasis.

K Nagaoka, K Fujii, H Zhang, K Usuda, G Watanabe, M Ivshina, J D Richter

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

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

54 citing papers in PubMed, 76 citations in OpenAlex.

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  20. Processing body (P-body) and its mediators in cancer.Molecular and cellular biochemistry · 2022
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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

7 authors at 2 institutions in 2 countries.

K NagaokaLaboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, Tokyo, Japan.
K FujiiLaboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, Tokyo, Japan.
H ZhangLaboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, Tokyo, Japan.
K UsudaLaboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, Tokyo, Japan.
G WatanabeLaboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, Tokyo, Japan.
M IvshinaProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
J D RichterProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Tokyo University of Agriculture and Technology · JPUniversity of Massachusetts Chan Medical School · US

Funding

POLYADENYLATION AND TRANSLATIONAL CONTROLR01GM046779 · NIGMS · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI RICHTER, JOEL D · 1992 to 2022
$7.7M
NIGMS NIH HHS R01 GM046779
6 · The paper itself

Abstract

In mouse mammary epithelial cells, cytoplasmic polyadenylation element binding protein 1 (CPEB1) mediates the apical localization of ZO-1 mRNA, which encodes a critical tight junction component. In mice lacking CPEB1 and in cultured cells from which CPEB has been depleted, randomly distributed ZO-1 mRNA leads to the loss of cell polarity. We have investigated whether this diminution of polarity results in an epithelial-to-mesenchyme (EMT) transition and possible increased metastatic potential. Here, we show that CPEB1-depleted mammary epithelial cells alter their gene expression profile in a manner consistent with an EMT and also become motile, which are made particularly robust when cells are treated with transforming growth factor-β, an enhancer of EMT. CPEB1-depleted mammary cells become metastatic to the lung following injection into mouse fat pads while ectopically expressed CPEB1 prevents metastasis. Surprisingly, CPEB1 depletion causes some EMT/metastasis-related mRNAs to have shorter poly(A) tails while other mRNAs to have longer poly(A) tails. Matrix metalloproteinase 9 (MMP9) mRNA, which encodes a metastasis-promoting factor, undergoes poly(A) lengthening and enhanced translation upon CPEB reduction. Moreover, in human breast cancer cells that become progressively more metastatic, CPEB1 is reduced while MMP9 becomes more abundant. These data suggest that at least in part, CPEB1 regulation of MMP9 mRNA expression mediates metastasis of breast cancer cells.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBreast NeoplasmsCell Line, TumorCell MovementFemaleHumansMammary Glands, AnimalMatrix Metalloproteinase 9MicemRNA Cleavage and Polyadenylation FactorsNeoplasm MetastasisPoly ARNA, MessengerTranscription FactorsTransforming Growth Factor betaCPEB1 protein, humanCpeb1 protein, mouseMatrix Metalloproteinase 9mRNA Cleavage and Polyadenylation FactorsPoly ARNA, MessengerTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID26411364
PMCPMC4809797
OpenAlexW2342398096

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.