Evidence map›Paper›PMID 37079213›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2023

Oncogenic roles of GPR176 in breast cancer: a potential marker of aggressiveness and a potential target of gene therapy.

Wen-Jing Yun, Hang Xue, Ning Yang, Li-Jun Xiao, Hong-Zhi Sun, Hua-Chuan Zheng

Open access · hybridAbstract read
In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Translational cancer research · 2026
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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

6 authors at 2 institutions in 1 country.

Wen-Jing YunDepartment of Oncology and Central Laboratory, The Affiliated Hospital of Chengde Medical University, Chengde, 067000, China.
Hang XueDepartment of Oncology and Central Laboratory, The Affiliated Hospital of Chengde Medical University, Chengde, 067000, China.
Ning YangDepartment of Oncology and Central Laboratory, The Affiliated Hospital of Chengde Medical University, Chengde, 067000, China.
Li-Jun XiaoDepartment of Immunology, Basic Medical College of Chengde Medical University, Chengde, 067000, China.
Hong-Zhi SunCancer Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, China.
Hua-Chuan ZhengDepartment of Oncology and Central Laboratory, The Affiliated Hospital of Chengde Medical University, Chengde, 067000, China. zheng_huachuan@hotmail.com.ORCID http://orcid.org/0000-0003-0965-6818
Chengde Medical University · CNJinzhou Medical University · CN

Funding

National Natural Scientific Foundation of China 81672700Natural Science Foundation of Hebei Province 21377772DNatural Science Foundation of Hebei Province H2022406034
6 · The paper itself

Abstract

backgroundBelonging to the G-protein coupled receptor 1 family, G protein-coupled receptor 176 (GPR176) is associated with the Gz/Gx G-protein subclass and is capable of decreasing cAMP production.

methodsGPR176 expression was detected by qRT-PCR, bioinformatics analysis, Western blot and immunohistochemistry, and compared with clinicopathological characteristics of breast cancer. GPR176-related genes and pathways were subjected to bioinformatic analysis. We also explored the effects of GPR176 on the phenotypes of breast cancer cells.

resultsLower expression of GPR176 mRNA was seen in breast cancer than in normal tissues, but the opposite pattern was found for its protein (p < 0.05). GPR176 mRNA was associated with female sex, low T staging, non-Her-2

conclusionThese results indicate that GPR176 might be involved in the tumorigenesis and subsequent progression of breast cancer by deteriorating aggressive phenotypes. It might be utilized as a potential biomarker to indicate the aggressive behaviors and poor prognosis of breast cancer and a potential target of genetic therapy.

Indexed as

Genetic TherapyNeoplasmsAnimalsBiomarkersCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticPhenotypePrognosisRNA, MessengerBiomarkersRNA, MessengerAggressivenessBreast cancerGPR176PrognosisTarget therapy

Identifiers

PMID37079213
PMCPMC10462518
OpenAlexW4366464109

What OpenQuestion holds

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LicenceCC BY
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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.