Evidence map›Paper›PMID 26988096›Full record

ArticleMolecular cancer2016

GLI pathogenesis-related 1 functions as a tumor-suppressor in lung cancer.

Xiumei Sheng, Nathan Bowen, Zhengxin Wang

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

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  6. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 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

3 authors at 2 institutions in 2 countries.

Xiumei ShengSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, 212013, China.
Nathan BowenThe Center for Cancer Research and Therapeutic Development, Department of Biological Sciences, Clark Atlanta University, 223 James P. Brawley Drive, S.W., Atlanta, Georgia, 30314, USA.
Zhengxin WangThe Center for Cancer Research and Therapeutic Development, Department of Biological Sciences, Clark Atlanta University, 223 James P. Brawley Drive, S.W., Atlanta, Georgia, 30314, USA. zwang@cau.edu.
Clark Atlanta University · USJiangsu University · CN

Funding

TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NIMHD NIH HHS 5G12MD007590NIMHD NIH HHS 5P20MD002285NIMHD NIH HHS G12 MD007590NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

backgroundGLI pathogenesis-related 1 (GLIPR1) was originally identified in glioblastomas and its expression was also found to be down-regulated in prostate cancer. Functional studies revealed both growth suppression and proapoptotic activities for GLIPR1 in multiple cancer cell lines. GLIPR1's role in lung cancer has not been investigated. Protein arginine methyltransferase 5 (PRMT5) is a protein arginine methyltransferase and forms a stoichiometric complex with the WD repeat domain 77 (WDR77) protein. Both PRMT5 and WDR77 are essential for growth of lung epithelial and cancer cells. But additional gene products that interact genetically or biochemichally with PRMT5 and WDR77 in the control of lung cancer cell growth are not characterized.

methodsDNA microarray and immunostaining were used to detect GLIPR1 expression during lung development and lung tumorigenesis. GLIPR1 expression was also analyzed in the TCGA lung cancer cohort. The consequence of GLIPR1 on growth of lung cancer cells in the tissue culture and lung tumor xenografts in the nude mice was observed.

resultsWe found that GLIPR1 expression is negatively associated with PRMT5/WDR77. GLIPR1 is absent in growing epithelial cells at the early stages of mouse lung development and highly expressed in the adult lung. Expression of GLIPR1 was down-regulated during lung tumorigenesis and its expression suppressed growth of lung cancer cells in the tissue culture and lung tumor xenografts in mice. GLIPR1 regulates lung cancer growth through the V-Erb-B avian erythroblastic leukemia viral oncogene homolog 3 (ErbB3).

conclusionsThis study reveals a novel pathway that PRMT5/WDR77 regulates GLIPR1 expression to control lung cancer cell growth and GLIPR1 as a potential therapeutic agent for lung cancer.

Indexed as

Genes, Tumor SuppressorAnimalsCarcinogenesisCell Line, TumorCell ProliferationDown-RegulationErb-b2 Receptor Tyrosine KinasesG1 Phase Cell Cycle CheckpointsG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansLungLung NeoplasmsMembrane ProteinsMice, NudeNeoplasm ProteinsErb-b2 Receptor Tyrosine KinasesGLIPR1 protein, humanMembrane ProteinsNeoplasm ProteinsNerve Tissue ProteinsReceptor, ErbB-3Transcription FactorsTransforming Growth Factor betaWDR77 protein, humanErbB3GLIPR1LungLung cancerPRMT5Tumor suppressorWDR77

Identifiers

PMID26988096
PMCPMC4797332
OpenAlexW2300537982

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.