Evidence map›Paper›PMID 25400079›Full record

ArticleScientific reports2014

Periostin suppression induces decorin secretion leading to reduced breast cancer cell motility and invasion.

Toshiyuki Ishiba, Makoto Nagahara, Tsuyoshi Nakagawa, Takanobu Sato, Toshiaki Ishikawa, Hiroyuki Uetake, Kenichi Sugihara, Yoshio Miki, Akira Nakanishi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 50 citations in OpenAlex.

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  8. False discovery rate control for high dimensional networks of quantile associations conditioning on covariates.Journal of the Royal Statistical Society. Series B, Statistical methodology · 2018
    Article
  9. Article
  10. Charting the unexplored extracellular matrix in cancer.International journal of experimental pathology · 2018
    Review
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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

9 authors at 2 institutions in 2 countries.

Toshiyuki Ishiba1] Department of Molecular Genetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU) [2] Department of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Makoto NagaharaDepartment of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Tsuyoshi NakagawaDepartment of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Takanobu SatoDepartment of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Toshiaki IshikawaDepartment of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Hiroyuki UetakeDepartment of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Kenichi SugiharaDepartment of Surgical Oncology, Tokyo Medical and Dental University (TMDU).
Yoshio Miki1] Department of Molecular Genetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU) [2] Department of Molecular Diagnosis, Cancer Institute, The Japanese Foundation of Cancer Research (JFCR).
Akira NakanishiDepartment of Molecular Genetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU).
Tokyo Medical and Dental University · JPCancer Institute (WIA) · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of cancer cells to metastasize is dependent on the interactions between their cell-surface molecules and the microenvironment. However, the tumor microenvironment, especially the cancer-associated stroma, is poorly understood. To identify proteins present in the stroma, we focused on phyllodes tumors, rare breast tumors that contain breast stromal cells. We compared the expression of proteins between phyllodes tumor and normal tissues using an iTRAQ-based quantitative proteomic approach. Decorin was expressed at reduced levels in phyllodes tumor tissues, whereas periostin was upregulated; this result was validated by immunohistochemical analysis of phyllodes tumors from 35 patients. Additionally, by immunoprecipitation and mass spectrometry, we confirmed that decorin forms a complex with periostin in both phyllodes tumors and BT-20 breast cancer cells. Following siRNA-mediated knockdown of periostin in T-47D cells, secreted decorin in the culture medium could be detected by multiple reaction monitoring (MRM). Furthermore, periostin knockdown in BT-20 cells and overexpression of decorin in MDA-MB-231 cells inhibited cell motility and invasion. Our results reveal the molecular details of the periostin-decorin complex in both phyllodes tumor tissues and breast cancer cells; this interaction may represent a novel target for anti-cancer therapy.

Indexed as

Breast NeoplasmsCell Adhesion MoleculesCell Line, TumorCell MovementDecorinFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPhyllodes TumorStromal CellsTumor MicroenvironmentCell Adhesion MoleculesDecorinPOSTN protein, human

Identifiers

PMID25400079
PMCPMC4233340
OpenAlexW2012951647

What OpenQuestion holds

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Registered trials

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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.