Evidence map›Paper›PMID 25153723›Full record

ArticleOncotarget2014

Anti-apoptotic effects of PCP4/PEP19 in human breast cancer cell lines: a novel oncotarget.

Taiji Hamada, Masakazu Souda, Takuya Yoshimura, Shoko Sasaguri, Kazuhito Hatanaka, Takashi Tasaki, Takako Yoshioka, Yasuyo Ohi, Sohsuke Yamada, Masato Tsutsui and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  6. CaMKK2 Promotes the Progression of Ovarian Carcinoma through the PI3K/PDK1/Akt Axis.Computational and mathematical methods in medicine · 2022
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  15. Article
  16. Identification of miRNA-mRNA crosstalk in CD4Journal of translational medicine · 2017
    Article
  17. Article
  18. 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

12 authors at 5 institutions in 1 country.

Taiji HamadaDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Masakazu SoudaDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Takuya YoshimuraDepartment of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Shoko SasaguriDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Kazuhito HatanakaDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Takashi TasakiDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Takako YoshiokaDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Yasuyo OhiDepartment of Pathology, Sagara Hospital, Social Medical Corporation Hakuaikai, Kagoshima, Japan.
Sohsuke YamadaDepartment of Pathology and Cell Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, 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.
Akihide TanimotoDepartment of Molecular and Cellular Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Kagoshima University · JPNational Sagamihara Hospital · JPTottori University · JPUniversity of Occupational and Environmental Health Japan · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PCP4/PEP19 is a calmodulin-binding anti-apoptotic peptide in neural cells but its potential role in human cancer has largely been unknown. We investigated the expression of PCP4/PEP19 in human breast cancer cell lines MCF-7, SK-BR-3, and MDA-MB-231 cells, and found that estrogen receptor (ER)-positive MCF-7 and ER-negative SK-BR-3 cells expressed PCP4/PEP19. In the MCF-7 cells, cell proliferation was estrogen-dependent, and PCP4/PEP19 expression was induced by estrogen. In both cell lines, PCP4/PEP19 knockdown induced apoptosis and slightly decreased Akt phosphorylation. Knockdown of calcium/calmodulin-dependent protein kinase kinase 1 (CaMKK1), resulting in decreased phospho-Akt(Thr308), enhanced apoptosis in SK-BR-3 but not in MCF-7 cells. CaMKK2 knockdown moderately decreased phospho-Akt(Thr308) and increased apoptosis in MCF-7 cells but not in SK-BR-3 cells. These data indicated that PCP4/PEP19 regulates apoptosis but exact mechanism is still unknown. PCP4/PEP19 can therefore potentially serve as independent oncotarget for therapy of PCP4/PEP19-positive breast cancers irrespective of ER expression.

Indexed as

ApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationFemaleHumansMCF-7 CellsMolecular Targeted TherapyNerve Tissue ProteinsPhosphorylationSignal TransductionTransfectionNerve Tissue ProteinsPCP4 protein, human

Identifiers

PMID25153723
PMCPMC4171614
OpenAlexW2130473927

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.