Evidence map›Paper›PMID 29348487›Full record

ArticleBritish journal of cancer2018

H1/pHGFK1 nanoparticles exert anti-tumoural and radiosensitising effects by inhibition of MET in glioblastoma.

Wenyan Zhang, Rui Duan, Jian Zhang, William K C Cheung, Xiaoge Gao, Raymond Zhang, Qing Zhang, Mengxue Wei, Gang Wang, Qian Zhang and 8 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 23 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

18 authors at 6 institutions in 2 countries.

Wenyan ZhangJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Rui DuanJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Jian ZhangJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
William K C CheungJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Xiaoge GaoJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Raymond ZhangDepartment of Biochemistry, Wheaton College, Norton, MA 02766, USA.
Qing ZhangJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Mengxue WeiJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Gang WangJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Qian ZhangJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Peng-Jin MeiThe Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002 People's Republic of China.
Hong-Lin ChenDepartment of Radiotherapy, The Oncological Hospital of Xuzhou, 131 Ring Road, Xuzhou, Jiangsu 221005, People's Republic of China.
Hsiangfu KungDepartment of Pathology, The South West Hospital, The Third Military Medical University, Chongqing 400038, People's Republic of China.
Marie C LinSchool of Medicine, Shenzhen University, Shenzhen, Guangdong 518060, People's Republic of China.
Zan ShenDepartment of Oncology, Affiliated Sixth People's Hospital, Shanghai Jiao Tong University, Shanghai 200240, People's Republic of China.
Junnian ZhengJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Longzhen ZhangThe Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002 People's Republic of China.
Hong YaoJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, People's Republic of China.
Xuzhou Medical College · CNArmy Medical University · CNJiangsu University · CNShanghai Jiao Tong University · CNShenzhen University · CNWheaton College - Massachusetts · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe therapeutic resistance to ionising radiation (IR) and anti-angiogenesis mainly impair the prognosis of patients with glioblastoma. The primary and secondary MET aberrant activation is one crucial factor for these resistances. The kringle 1 domain of hepatocyte growth factor (HGFK1), an angiogenic inhibitor, contains a high-affinity binding domain of MET; however, its effects on glioblastoma remain elusive.

methodsWe formed the nanoparticles consisting of a folate receptor-targeted nanoparticle-mediated HGFK1 gene (H1/pHGFK1) and studied its anti-tumoural and radiosensitive activities in both subcutaneous and orthotopic human glioma cell-xenografted mouse models. We then elucidated its molecular mechanisms in human glioblastoma cell lines in vitro.

resultsWe demonstrated for the first time that peritumoural injection of H1/pHGFK1 nanoparticles significantly inhibited tumour growth and prolonged survival in tumour-bearing mice, as well as enhanced the anti-tumoural efficacies of IR in vivo by reducing Ki-67 expression, enhancing TUNEL staining-indicated apoptotic indexes, reducing microvascular intensity and reversing IR-induced MET overexpression in tumour tissues. Furthermore, we showed that HGFK1 suppressed the proliferation and induced cell apoptosis and enhanced sensitivity to IR in glioblastoma cell lines, mainly by suppressing the activities of MET receptor, down-regulating ATM-Chk2 axis but up-regulating Chk1.

conclusionsH1/pHGFK1 exerts anti-tumoural and radiosensitive activities mainly through the inhibition and reversal of IR-induced MET and ATM-Chk2 axis activities in glioblastoma. H1/pHGFK1 nanoparticles are a potential radiosensitiser and angiogenic inhibitor for glioblastoma treatment.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticGlioblastomaHepatocyte Growth FactorHumansKringlesMiceNanoparticlesPlasmidsProto-Oncogene Proteins c-metRadiation-Sensitizing AgentsXenograft Model Antitumor AssaysHepatocyte Growth FactorHGF protein, humanMET protein, humanProto-Oncogene Proteins c-metRadiation-Sensitizing Agents

Identifiers

PMID29348487
PMCPMC5830599
OpenAlexW2784099351

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.