Evidence map›Paper›PMID 27551446›Full record

ArticleCell death discovery2015

Modulation of dendritic cell function by the radiation-mediated secretory protein γ-synuclein.

S-M Kang, M-H Kim, K-H Song, S-Y Jung, J Ahn, S-G Hwang, J-H Lee, D-S Lim, J-Y Song

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

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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 1 country.

S-M KangDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
M-H KimDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
K-H SongDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
S-Y JungDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
J AhnDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
S-G HwangDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
J-H LeeDepartment of Biotechnology, CHA University , Seongnam 463-400, Republic of Korea.
D-S LimDepartment of Biotechnology, CHA University , Seongnam 463-400, Republic of Korea.
J-Y SongDivision of Radiation Cancer Sciences, Korea Institute of Radiological and Medical Sciences , Seoul 139-706, Republic of Korea.
Korea Institute of Radiological and Medical Sciences · KRCHA University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, γ-synuclein (SNCG), which is also known as breast cancer-specific gene-1, has been demonstrated to be an adverse and aggressive marker in breast cancer. In our previous study, SNCG was significantly upregulated in irradiated human breast cancer cells. The aim of this study was to investigate whether radiation-induced, tumor-derived SNCG can influence dendritic cell (DC) function in immune systems. The phenotypical and functional changes of DCs in the presence or absence of SNCG were investigated by FACS analysis, ELISA, and real-time PCR. The ability of SNCG-treated DCs to influence T cells was also examined by coculturing with T cells. The treatment of DCs with SNCG protein inhibited the surface expression of the co-stimulatory molecules CD40 and CD86, and decreased the mRNA levels of pro-inflammatory cytokines. The SNCG-treated DCs inhibited T-cell proliferation slightly, but distinctively increased the population of regulatory T cells. In addition, the production of TGF-β from T cells was significantly increased when they were cocultured with SNCG-treated DCs. Taken together, these results demonstrate that tumor-derived SNCG contributes to immunosuppressive effects via the inhibition of DC differentiation and activation, thus making it a potential target for cancer treatment.

Identifiers

PMID27551446
PMCPMC4979407
OpenAlexW2528986999

What OpenQuestion holds

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LicenceCC BY
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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.