Evidence map›Paper›PMID 27855669›Full record

ArticleBMC cancer2016

Expression of Par3 polarity protein correlates with poor prognosis in ovarian cancer.

Hiroe Nakamura, Kazunori Nagasaka, Kei Kawana, Ayumi Taguchi, Yuriko Uehara, Mitsuyo Yoshida, Masakazu Sato, Haruka Nishida, Asaha Fujimoto, Tomoko Inoue and 6 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 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
1.3field-weighted citation impact, top 20% 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, 28 citations in OpenAlex.

  1. Article
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  7. Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022
    Review
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  15. Loss of TDP43 inhibits progression of triple-negative breast cancer in coordination with SRSF3.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. From Neural Crest Development to Cancer and Vice Versa: How p75Frontiers in molecular neuroscience · 2018
    Review
  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

16 authors at 1 institution in 1 country.

Hiroe NakamuraDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Kazunori NagasakaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. nagasakak-tky@umin.ac.jp.ORCID 0000-0002-0696-5175
Kei KawanaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. kkawana-tky@umin.org.
Ayumi TaguchiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yuriko UeharaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Mitsuyo YoshidaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Masakazu SatoDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Haruka NishidaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Asaha FujimotoDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Tomoko InoueDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Katsuyuki AdachiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Takeshi NagamatsuDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Takahide ArimotoDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Katsutoshi OdaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yutaka OsugaDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Tomoyuki FujiiDepartment of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have shown that the cell polarity protein partitioning defective 3 (Par3) plays an essential role in the formation of tight junctions and definition of apical-basal polarity. Aberrant function of this protein has been reported to be involved in epithelial-mesenchymal transition (EMT) and cancer invasion. The aim of this study was to examine the functional mechanism of Par3 in ovarian cancer.

methodsFirst, we investigated the association between Par3 expression level and survival of 50 ovarian cancer patients. Next, we conducted an in vitro analysis of ovarian cancer cell lines, focusing on the cell line JHOC5, to investigate Par3 function. To investigate the function of Par3 in invasion, the IL-6/STAT3 pathway was analyzed upon Par3 knockdown with siRNA. The effect of siRNA treatment was assessed by qPCR, ELISA, and western blotting. Invasiveness and cell proliferation following treatment with siRNA against Par3 were investigated using Matrigel chamber, wound healing, and cell proliferation assays.

resultsExpression array data for ovarian cancer patient samples revealed low Par3 expression was significantly associated with good prognosis. Univariate analysis of clinicopathological factors revealed significant association between high Par3 levels and peritoneal dissemination at the time of diagnosis. Knockdown of Par3 in JHOC5 cells suppressed cell invasiveness, migration, and cell proliferation with deregulation of IL-6/STAT3 activity.

conclusionTaken together, these results suggest that Par3 expression is likely involved in ovarian cancer progression, especially in peritoneal metastasis. The underlying mechanism may be that Par3 modulates IL-6 /STAT3 signaling. Here, we propose that the expression of Par3 in ovarian cancer may control disease outcome.

Indexed as

Adaptor Proteins, Signal TransducingAdultAgedAged, 80 and overCell Cycle ProteinsCell Line, TumorCell ProliferationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInterleukin-6Membrane ProteinsMiddle AgedNeoplasm InvasivenessOligonucleotide Array Sequence AnalysisAdaptor Proteins, Signal TransducingCell Cycle ProteinsIL6 protein, humanInterleukin-6Membrane ProteinsPARD3 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorIL-6Ovarian cancerPar3STAT3

Identifiers

PMID27855669
PMCPMC5114836
OpenAlexW2555511427

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.