Evidence map›Paper›PMID 30068373›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Overexpression of the Kininogen-1 inhibits proliferation and induces apoptosis of glioma cells.

Jinfang Xu, Jun Fang, Zhonghao Cheng, Longlong Fan, Weiwei Hu, Feng Zhou, Hong Shen

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 84 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

7 authors at 2 institutions in 1 country.

Jinfang XuDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang Province, 310009, China.
Jun FangDepartment of Radiotherapy, Zhejiang Cancer Hospital, No.1 East Banshan Road, Gongshu District, Hangzhou, Zhejiang Province, 310022, China.
Zhonghao ChengDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang Province, 310009, China.
Longlong FanDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang Province, 310009, China.
Weiwei HuDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang Province, 310009, China.
Feng ZhouDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang Province, 310009, China. fengz_zhouf@163.com.
Hong ShenDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang Province, 310009, China.
Second Affiliated Hospital of Zhejiang University · CNZhejiang Cancer Hospital · CN

Funding

Natural Science Foundation of Zhejiang Province LY17H160016Research Project of Zhejiang Provincial Health Department 2012KYA104
6 · The paper itself

Abstract

backgroundGlioma is the most common primary central nervous system tumor derived from glial cells. Kininogen-1 (KNG1) can exert antiangiogenic properties and inhibit proliferation of endothelial cells. The effect of KNG1 on the glioma is rarely reported, so our purpose in to explore its mechanism in glioma cells.

methodsThe differentially expressed genes (DEGs) were identified based on The Cancer Genome Atlas (TCGA) database. The KNG1-vector was transfected into the two glioma cells. The viability, apoptosis and cell cycle of glioma cells and microvessel density (MVD) were detected by cell counting kit-8 assay, flow cytometry and immunohistochemistry, respectively. The expression were measured by quantitative real-time PCR and Western blot, respectively. A tumor mouse model was established to determine apoptosis rate of brain tissue by terminal deoxynucleotidyl transfer-mediated dUTP nick end labeling (TUNEL) analysis.

resultsKNG1 was identified as the core gene and lowly expressed in the glioma cells. Overexpression of KNG1 inhibited cell viability and angiogenesis of glioma cells. Overexpression of KNG1 promoted the apoptosis and G1 phase cell cycle arrest of glioma cells. Moreover, the expressions of VEGF, cyclinD1, ki67, caspase-3/9 and XIAP were regulated by overexpression of KNG1. In addition, overexpression of KNG1 inhibited the activity of PI3K/Akt. Furthermore, overexpression of KNG1 decreased the tumor growth and promoted the apoptosis of decreased by overexpression of KNG1 in vivo. .

conclusionsOverexpression of KNG1 suppresses glioma progression by inhibiting the proliferation and promoting apoptosis of glioma cells, providing a therapeutic strategy for the malignant glioma.

Indexed as

AnimalsApoptosisBrain NeoplasmsCell Line, TumorCell ProliferationFemaleGliomaHeterograftsHumansKininogensMaleMiceMice, NudeMiddle AgedTransfectionKininogensKNG1 protein, humanAngiogenesisApoptosisGliomaKNG1

Identifiers

PMID30068373
PMCPMC6090912
OpenAlexW2886933640

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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.