Evidence map›Paper›PMID 27384474›Full record

ArticleOncotarget2016

PCP4/PEP19 promotes migration, invasion and adhesion in human breast cancer MCF-7 and T47D cells.

Takuya Yoshimura, Taiji Hamada, Hiroshi Hijioka, Masakazu Souda, Kazuhito Hatanaka, Takako Yoshioka, Sohsuke Yamada, Masato Tsutsui, Yoshihisa Umekita, Norifumi Nakamura and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
0.5field-weighted citation impact, top 30% 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, 25 citations in OpenAlex.

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  15. Ubiquitin-specific protease 7 downregulation suppresses breast cancer in vitro.Turkish journal of biology = Turk biyoloji dergisi · 2020
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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

11 authors at 4 institutions in 1 country.

Takuya YoshimuraDepartment of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Taiji HamadaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Hiroshi HijiokaDepartment of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Masakazu SoudaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Kazuhito HatanakaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Takako YoshiokaDepartment of Pathology, Children's Cancer Center, National Center for Child Health and Development, Tokyo, Japan.
Sohsuke YamadaDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Masato TsutsuiDepartment of Pharmacology, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan.
Yoshihisa UmekitaDivision of Organ Pathology, Faculty of Medicine, Tottori University, Yonago, Japan.
Norifumi NakamuraDepartment of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Akihide TanimotoDepartment of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Kagoshima University · JPNational Center For Child Health and Development · JPTottori University · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purkinje cell protein (PCP) 4/peptide (PEP) 19 is expressed in Purkinje cells where it has a calmodulin-binding, anti-apoptotic function. We recently demonstrated that PCP4/PEP19 is expressed and inhibit apoptosis in human breast cancer cell lines. In the present study we investigated the role of PCP4/PEP19 in cell morphology, adhesion, migration, and invasion in MCF-7 and T47D human breast cancer cell lines. Knockdown of PCP4/PEP19 reduced the formation of filopodia-like cytoplasmic structures and vinculin expression, and enhanced E-cadherin expression. Activities of migration, invasion, and cell adhesion were also decreased after the knockdown of PCP4/PEP19 in MCF-7 and T47D cells. These results suggested that PCP4/PEP19 promotes cancer cell adhesion, migration, and invasion and that PCP4/PEP19 may be a potential target for therapeutic agents in breast cancer treatment which act by inhibiting epithelial-mesenchymal transition and enhancing apoptotic cell death.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBreast NeoplasmsCadherinsCell AdhesionCell CountCell Line, TumorCell MovementCulture MediaEpithelial-Mesenchymal TransitionFemaleHumansMCF-7 CellsNeoplasm InvasivenessNerve Tissue ProteinsPolycomb Repressive Complex 1BMI1 protein, humanCadherinsCulture MediaNerve Tissue ProteinsPCP4 protein, humanPolycomb Repressive Complex 1RNA, Small InterferingVinculinbreast cancerEMTinvasionmigrationPCP4/PEP19

Identifiers

PMID27384474
PMCPMC5226490
OpenAlexW2493007832

What OpenQuestion holds

Textmetadata
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.