Evidence map›Paper›PMID 31560089›Full record

ArticleMedical oncology (Northwood, London, England)2019

Mechanism of VIPR1 gene regulating human lung adenocarcinoma H1299 cells.

Lufeng Zhao, Zipu Yu, Baiqin Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  8. [VIPR1 promoter methylation promotes transcription factor AP-2Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
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  9. MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1.Computational and mathematical methods in medicine · 2022
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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

3 authors at 1 institution in 1 country.

Lufeng ZhaoDepartment of Thoracic Surgery, Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Shangcheng District, Hangzhou, 310009, China.
Zipu YuDepartment of Thoracic Surgery, Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Shangcheng District, Hangzhou, 310009, China.
Baiqin ZhaoDepartment of Thoracic Surgery, Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Shangcheng District, Hangzhou, 310009, China. 2196024@zju.edu.cn.ORCID http://orcid.org/0000-0001-8768-0042
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vasoactive intestinal peptide receptor-1(VIPR1) has prominent growth effects on a number of common neoplasms. However, there were contradictions in the effect cross different cancers. We aimed to explore the effect of VIPR1 overexpression on a human lung adenocarcinoma cell line H1299. GEO dataset was used to screen differentially expressed genes in lung adenocarcinoma tissues. The expression of VIPR1 mRNA was determined in the cancer Genome Atlas (TCGA). Immunohistochemical analysis was performed to determine VIPR1 protein expression in lung adenocarcinoma and corresponding adjacent tissues (n = 22). Fluorescence real-time quantitative PCR detected the expression of VIPR1 in human normal lung epithelial cell line BEAS-2B and lung adenocarcinoma cell line H1299. Overexpression strategies were employed to assess functions of VIPR1 expression on several malignant phenotypes in H1299. The expression of VIPR1 was lower in lung adenocarcinoma tissues than that in adjacent tissues. Compared with the normal lung epithelial cells BEAS-2B, VIPR1 was down-regulated in lung cancer cells H1299 (P < 0.05). After the overexpression of VIPR1, we found that VIPR1 significantly inhibited growth, migration, and invasion of H1299 cells (P < 0.05). Our findings point out the tumor suppressor roles of VIPR1 in human LUAD pathogenesis.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinoma of LungAdultAgedCell Line, TumorCell MovementCell ProliferationFemaleGenes, Tumor SuppressorHumansMaleMiddle AgedNeoplasm StagingReceptors, Vasoactive Intestinal Polypeptide, Type IRNA, MessengerUp-RegulationReceptors, Vasoactive Intestinal Polypeptide, Type IRNA, MessengerVIPR1 protein, humanLung adenocarcinomaMigration and invasionProliferationVIPR1

Identifiers

PMID31560089
OpenAlexW2975213011

What OpenQuestion holds

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Read underepoch 390

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.