Evidence map›Paper›PMID 26760963›Full record

ArticleOncotarget2016

GPR171 expression enhances proliferation and metastasis of lung cancer cells.

So Hee Dho, Kwang-Pyo Lee, Dongjun Jeong, Chang-Jin Kim, Kyung-Sook Chung, Ji Young Kim, Bum-Chan Park, Sung Sup Park, Seon-Young Kim, Ki-Sun Kwon

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. GPCRs: emerging targets for novel T cell immune checkpoint therapy.Cancer immunology, immunotherapy : CII · 2024
    Review
  4. Article
  5. Development of anMolecular therapy. Methods & clinical development · 2023
    Article
  6. Article
  7. TubularInternational journal of molecular sciences · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
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.

So Hee DhoAging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Kwang-Pyo LeeAging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Dongjun JeongDepartment of Pathology, College of Medicine Soonchunhyang University, Chonan 330-090, Republic of Korea.
Chang-Jin KimDepartment of Pathology, College of Medicine Soonchunhyang University, Chonan 330-090, Republic of Korea.
Kyung-Sook ChungGenome Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Ji Young KimAging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Bum-Chan ParkAging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Sung Sup ParkAging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Seon-Young KimGenome Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Ki-Sun KwonAging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea.
Korea Research Institute of Bioscience and Biotechnology · KRSoonchunhyang University · KRKorea University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) are among the most significant therapeutic targets and some of them promote the growth and metastasis of cancer. Here, we show that an increase in the levels of GPR171 is crucial for lung cancer tumor progression in vitro and in vivo. Immunostaining of clinical samples indicated that GPR171 was overexpressed in 46.8% of lung carcinoma tissues. Depletion of GPR171 with an anti-GPR171 antibody decreased proliferation of lung carcinoma cells and attenuated tumor progression in a mouse xenograft model. Knockdown of GPR171 also inhibited migration and invasion of the lung cancer cell lines. Notably, inhibition of GPR171 synergistically enhanced the tumoricidal activity of an epidermal growth factor receptor (EGFR) inhibitor in lung cancer cells. These results indicate that GPR171 blockade is a promising antineoplastic strategy and provide a preclinical rationale for combined inhibition of GPR171 and EGFR.

Indexed as

Cell MovementCell ProliferationAnimalsApoptosisBlotting, WesternCarcinoma, Non-Small-Cell LungFemaleHumansImmunoenzyme TechniquesLung NeoplasmsMiceMice, Inbred BALB CMice, NudeNeoplasm StagingPrognosisReceptors, G-Protein-CoupledReceptors, G-Protein-CoupledEGFRGPCRGPR171lung cancer

Identifiers

PMID26760963
PMCPMC4884959
OpenAlexW2236539942

What OpenQuestion 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 OpenQuestion graph.