Evidence map›Paper›PMID 35117030›Full record

ArticleTranslational cancer research2019

ADAMTS-1 inhibits angiogenesis via the PI3K/Akt-eNOS-VEGF pathway in lung cancer cells.

Bu Wang, Shuo Chen, Jian-Qing Zhao, Bao-Li Xiang, Xin Gu, Fang Zou, Zhi-Hua Zhang

Open access · diamondAbstract read
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Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-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

21 citing papers in PubMed, 28 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.

Bu WangDepartment of Respiratory Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Shuo ChenDepartment of Respiratory Medicine, The Hospital of 81st Group Army PLA, Zhangjiakou 075000, China.
Jian-Qing ZhaoDepartment of Respiratory Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Bao-Li XiangDepartment of Respiratory Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Xin GuDepartment of Neurology, The First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Fang ZouDepartment of Respiratory Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Zhi-Hua ZhangDepartment of Respiratory Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
Hebei North University · CN175th Hospital of People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundADAMTS-1 (a disintegrin and metalloproteinase with thrombospondin repeats-1) is a recently characterized protein containing a metalloproteinase domain, a disintegrin-like domain and a thrombospondin type 1 motif, which is involved in angiogenesis. However, the roles of ADAMTS-1 in angiogenesis of lung cancer (LC) remain unclear.

methodsThe mRNA expression of ADAMTS-1 and VEGF was examined by qRT-PCR. Western blots were used to detect the protein expression of ADAMTS-1 and vascular endothelial growth factor (VEGF) in A549 cells and to analyse the cellular effect of a PI3K/Akt activator and an endothelial nitric oxide synthase (eNOS) activator. ADAMTS-1 and VEGF contents in cell culture supernatants were measured by ELISA. Cell viability, cell cycle, migration, and angiogenesis of HUVECs were evaluated by MTT assay, flow cytometry, scratch assay and tube formation assay, respectively.

resultsOur data revealed that the expression of ADAMTS-1 was downregulated, while the expression of VEGF was upregulated in A549 cells. Decreased ADAMTS-1 content was also detected in A549 cell culture supernatant. Overexpression of ADAMTS-1 inhibited VEGF expression and A549 cell proliferation. Moreover, ADAMTS-1 overexpression repressed proliferation, migration and angiogenesis of HUVECs. Mechanistically, ADAMTS-1 suppressed the expression of VEGF in HUVECs by inhibiting PI3K/Akt-eNOS, while a PI3K activator and an eNOS activator each partly reversed the expression of VEGF. In addition, activation of the PI3K/Akt pathway or VEGF overexpression reversed the inhibitory effect of ADAMTS-1 overexpression on HUVECs angiogenesis.

conclusionsThese results indicated that ADAMTS-1 inhibited angiogenesis of LC cells via regulation of the PI3K/Akt-eNOS/VEGF axis, which shed light on LC pathogenesis and provided potential targets for LC therapy.

Indexed as

ADAMTS-1angiogenesislung cancer (LC)PI3K/Akt-eNOSvascular endothelial growth factor (VEGF)

Identifiers

PMID35117030
PMCPMC8798392
OpenAlexW2990267864

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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.