Evidence map›Paper›PMID 32647670›Full record

ArticleAnnals of translational medicine2020

The role of GPR110 in lung cancer progression.

Benting Ma, Junjie Zhu, Jieakesu Su, Feng Pan, Yuan Ji, Lijuan Luan, Jie Huang, Yingyong Hou

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. G protein-coupled receptors: a gateway to targeting oncogenic EVs?Extracellular vesicles and circulating nucleic acids · 2024
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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

8 authors at 5 institutions in 1 country.

Benting MaDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Junjie ZhuThoracic Surgery Laboratory, Shanghai Pulmonary Hospital Affiliated to Tong Ji University School of Medicine, Shanghai, China.
Jieakesu SuDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Feng PanThoracic Surgery Laboratory, Shanghai Pulmonary Hospital Affiliated to Tong Ji University School of Medicine, Shanghai, China.
Yuan JiDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Lijuan LuanDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Jie HuangDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yingyong HouDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
The First Affiliated Hospital, Sun Yat-sen University · CNShanghai Pulmonary Hospital · CNFudan University · CNSun Yat-sen University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundG protein-coupled receptors (GPCRs) are involved in several signaling pathways. However, the roles of many GPCRs in tumor oncogenesis and progression are not fully understood. In our previous study, we concluded that the absence of Gpr110 decelerates the development of liver brosis/cirrhosis into tumorigenesis. In our current study, the role of GPR110 in the oncogenesis and progression of lung cancer was observed.

methodsAfter collecting tumor tissues from lung cancer patients, the expression of GPR110 was analyzed by both Western blotting and real-time PCR. Immunofluorescence was used to observe GPR110 expression in human lung cancer cells. A CCK8 kit was used to analyze the proliferation of human lung cancer cells transfected with Gpr110. Changes in cell migration were evaluated with wound healing and Transwell assays. A nude mouse xenograft model was constructed. Lung cancer model was induced in Gpr110

resultsGPR110 mRNA and protein expression was significantly higher in lung cancer tissue. GPR110 was barely expressed in H460, A549, H1299, and SPC-A1 cells, but its expression in PC-9 and QG56 cells was significantly higher. Overexpression of GPR110 promoted the proliferation and cell aggregation of H1299 cells and H1299 cell migration was also enhanced. Overexpression of GPR110 in H1299 cells significantly promoted tumor development in the nude mice tumor xenograft model. There was no statistical significance between the Gpr110

conclusionsOur findings indicate that GPR110 promotes the progression of lung cancer through accelerating cell proliferation and migration.

Indexed as

Gpr110lung cancerurethaneXenograft model

Identifiers

PMID32647670
PMCPMC7333099
OpenAlexW3034550599

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.