Evidence map›Paper›PMID 27765922›Full record

ArticleOncotarget2016

G-protein-coupled receptor 81 promotes a malignant phenotype in breast cancer through angiogenic factor secretion.

Yu Jin Lee, Kyeong Jin Shin, Soo-Ah Park, Kyeong Su Park, Seorim Park, Kyun Heo, Young-Kyo Seo, Dong-Young Noh, Sung Ho Ryu, Pann-Ghill Suh

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

94 citing papers in PubMed, 140 citations in OpenAlex.

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34 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Yu Jin LeeSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Kyeong Jin ShinSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Soo-Ah ParkSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Kyeong Su ParkSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Seorim ParkSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Kyun HeoNew Experimental Therapeutics Branch, Division of Convergence Technology, National Cancer Center, Goyang-si, Republic of Korea.
Young-Kyo SeoSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Dong-Young NohDepartment of Surgery, Seoul National University, College of Medicine, Seoul, Republic of Korea.
Sung Ho RyuDepartment of Life Science, Pohang University of Science and Technology (POSTECH), San31, Hyoja Dong, Pohang, Republic of Korea.
Pann-Ghill SuhSchool of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.
Ulsan National Institute of Science and Technology · KRPohang University of Science and Technology · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G-protein-coupled receptor 81 (GPR81) functions as a receptor for lactate and plays an important role in the regulation of anti-lipolytic effects in adipocytes. However, to data, a role for GPR81 in the tumor microenvironment has not been clearly defined. Here, GPR81 expression in breast cancer patients and several breast cancer cell lines was significantly increased compared with normal mammary tissues and cells. GPR81 knockdown resulted in impaired breast cancer growth and led to apoptosis both in vitro and in vivo. Furthermore, the inhibition of GPR81 signaling suppressed angiogenesis through a phosphoinositide 3-OH kinase (PI3K)/Akt-cAMP response element binding protein (CREB) pathway, which led to decreased production of the pro-angiogenic mediator amphiregulin (AREG). Overall, these findings identify GPR81 as a tumor-promoting receptor in breast cancer progression and suggest a novel mechanism that regulates GPR81-dependent activation of the PI3K/Akt signaling axis in tumor microenvironment.

Indexed as

Tumor MicroenvironmentAmphiregulinAnimalsApoptosisBreastBreast NeoplasmsCell Line, TumorCell ProliferationCell SeparationCyclic AMP Response Element-Binding ProteinFemaleFlow CytometryGene Knockdown TechniquesHumansLactic AcidMiceAmphiregulinAREG protein, humanCyclic AMP Response Element-Binding ProteinHCAR1 protein, humanLactic AcidPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledRNA, Small InterferingAktamphiregulinangiogenesisbreast cancerGPR81

Identifiers

PMID27765922
PMCPMC5342597
OpenAlexW2524915496

What Socratic holds

Textmetadata
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 Socratic graph.