Evidence map›Paper›PMID 27861149›Full record

ArticleOncotarget2017

AAV-Mediated angiotensin 1-7 overexpression inhibits tumor growth of lung cancer in vitro and in vivo.

Xinglu Chen, Sansan Chen, Nana Pei, Yingying Mao, Shengyao Wang, Renhe Yan, Na Bai, Andrew Li, Yanling Zhang, Hongyan Du and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. 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
2.1field-weighted citation impact, top 11% 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, 22 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

14 authors at 6 institutions in 2 countries.

Xinglu ChenSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Sansan ChenDepartment of Urology, The First Affiliated Hospital of Clinical Medicine of Guangdong Pharmaceutical University, Guangzhou, Guangdong, China.
Nana PeiDepartment of Clinical Pathology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Yingying MaoSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Shengyao WangSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Renhe YanSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Na BaiDeparement of Nuclear Medicine, People's Hospital of Yuxi City, Yuxi, Yunnan, China.
Andrew LiDepartment of Biomedical Engineering, The Johns University School of Medicine, Baltimore, USA.
Yanling ZhangSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Hongyan DuSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Baihong ChenSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Colin SumnersDepartments of Physiology and Functional Genomics, University of Florida, Gainesville, Florida, USA.
Jinlong LiSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Hongwei LiSchool of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Southern Medical University · CNFirst Affiliated Hospital of Guangdong Pharmaceutical University · CNFirst Affiliated Hospital of Jinan University · CNJohns Hopkins Medicine · USSixth Affiliated Hospital of Kunming Medical University · CNUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ang-(1-7) inhibits lung cancer cell growth both in vitro and in vivo. However, the molecular mechanism of action is unclear and also the rapid degradation of Ang-(1-7) in vivo limits its clinical application. Here, we have demonstrated that Ang- (1-7) inhibits lung cancer cell growth by interrupting pre-replicative complex assembly and restrains epithelial-mesenchymal transition via Cdc6 inhibition. Furthermore, we constructed a mutant adeno-associated viral vector AAV8 (Y733F) that produced stable and high efficient Ang-(1-7) expression in a xenograft tumor model. The results show that AAV8-mediated Ang-(1-7) over-expression can remarkably suppress tumor growth in vivo by down-regulating Cdc6 and anti-angiogenesis. Ang-(1-7) over-expression via the AAV8 method may be a promising strategy for lung cancer treatment.

Indexed as

Angiotensin IAnimalsCarcinoma, Non-Small-Cell LungCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDependovirusDNA ReplicationDown-RegulationEpithelial-Mesenchymal TransitionFemaleGenetic VectorsHumansImmunohistochemistryLungAngiotensin Iangiotensin I (1-7)CDC6 protein, humanCell Cycle ProteinsMultienzyme ComplexesNuclear ProteinsPeptide FragmentsVascular Endothelial Growth Factor AVEGFA protein, humanadeno-associated viral vectorAng-(1-7)DNA synthesislung cancerproliferation

Identifiers

PMID27861149
PMCPMC5352125
OpenAlexW2556348543

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.