Evidence map›Paper›PMID 32735635›Full record

ArticlePloS one2020

Selenoprotein P inhibits cell proliferation and ROX production in HCC cells.

Jianxin Wang, Pei Shen, Sha Liao, Lian Duan, Dandan Zhu, Jinling Chen, Liuting Chen, Xiaolei Sun, Yinong Duan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. 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 1 institution in 1 country.

Jianxin WangDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, People's Republic of China.
Pei ShenDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, People's Republic of China.
Sha LiaoDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, People's Republic of China.
Lian DuanDepartment of Medical Informatics, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Dandan ZhuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Jinling ChenDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Liuting ChenDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Xiaolei SunDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.
Yinong DuanDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, People's Republic of China.ORCID 0000-0001-5824-5762
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Selenoprotein P (SEPP1) is a kind of secretory glycoproteins with an antioxidant effect during the development of some diseases. In this study, we attempted to observe the expression of SEPP1 in livers from the patients with hepatocellular carcinoma (HCC) and explore its effect on HCC cells. All the tissues from patients with HCC were obtained from Affiliated Hospital of Nantong University. Western blot and immunohistochemical results showed that SEPP1 was reduced in HCC liver tissues. Its expression was negatively correlated with Ki67 expression in tissues. The expression of SEPP1 in normal liver cell line was significantly higher than those in the liver cancer cell lines. Serum starvation and release experiment demonstrated that SEPP1 expression was reduced and PCNA expression was increased, when the serum was re-added into cell culture system and the cells were on a proliferation state. After SEPP1 over-expression plasmid was transfected into HepG2 cells, cell proliferation of HepG2 cells and PCNA expression level were all inhibited by SEPP1. Results obtained via 8-isoprostane ELISA further indicated that inhibited ROS level was found in HepG2 cells transfected with SEPP1 over-expression plasmid. In addition, RT-qPCR results demonstrated that GPX1 expression levels increased in HepG2 cells transfected with SEPP1 over-expression plasmid. In conclusion, SEPP1 may inhibit the proliferation of HCC cells, accompanied by the reduction of ROS production and the increasing of GPX1 expression.

Indexed as

Carcinoma, HepatocellularCell ProliferationFemaleGene Expression Regulation, NeoplasticGlutathione PeroxidaseGlutathione Peroxidase GPX1Hep G2 CellsHumansKi-67 AntigenLiverLiver NeoplasmsMaleSelenoprotein PGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanKi-67 AntigenMKI67 protein, humanSELENOP protein, humanSelenoprotein P

Identifiers

PMID32735635
PMCPMC7394388
OpenAlexW3046437965

What OpenQuestion holds

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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 OpenQuestion graph.