Evidence map›Paper›PMID 33298014›Full record

ArticleBMC cancer2020

Gene expression analysis of human prostate cell lines with and without tumor metastasis suppressor CD82.

Pushpaja Dodla, Vanitha Bhoopalan, Sok Kean Khoo, Cindy Miranti, Suganthi Sridhar

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  4. Stromal-epithelial interaction inducesFrontiers in oncology · 2023
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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

5 authors at 3 institutions in 1 country.

Pushpaja DodlaDepartment of Cell and Molecular Biology, Grand Valley State University, Allendale, MI, 49401, USA.
Vanitha BhoopalanDepartment of Cell and Molecular Biology, Grand Valley State University, Allendale, MI, 49401, USA.
Sok Kean KhooDepartment of Cell and Molecular Biology, Grand Valley State University, Allendale, MI, 49401, USA.
Cindy MirantiDepartment of Cellular and Molecular Medicine, University of Arizona Cancer Center, University of Arizona, Tucson, AZ, 85724, USA.
Suganthi SridharDepartment of Integrative Biology, University of South Florida, 140, 7Th Avenue S, University of South Florida, St. Petersburg, FL, 33701, USA. suganthi@usf.edu.ORCID http://orcid.org/0000-0003-1422-4868
Grand Valley State University · USUniversity of Arizona · USUniversity of South Florida St. Petersburg · US

Funding

Graduate School, Grand Valley State University (US) Graduate School Presidential awardGraduate School, Grand Valley State University(US) Graduate School Presidential AwardUniversity of South Florida, St.Petersburg(US) Internal Start-up grantWest Michigan Science and Technology Initiative and Grand Valley State University(US) Grand Valley State University Center for Scholarly and Creative Excellence Catalyst Grant
6 · The paper itself

Abstract

backgroundTetraspanin CD82 is a tumor metastasis suppressor that is known to down regulate in various metastatic cancers. However, the exact mechanism by which CD82 prevents cancer metastasis is unclear. This study aims to identify genes that are regulated by CD82 in human prostate cell lines.

methodsWe used whole human genome microarray to obtain gene expression profiles in a normal prostate epithelial cell line that expressed CD82 (PrEC-31) and a metastatic prostate cell line that does not express CD82 (PC3). Then, siRNA silencing was used to knock down CD82 expression in PrEC-31 while CD82 was re-expressed in PC3 to acquire differentially-expressed genes in the respective cell line.

resultsDifferentially-expressed genes with a P < 0.05 were identified in 3 data sets: PrEC-31 (+CD82) vs PrEC-31(-CD82), PC3-57 (+CD82) vs. PC3-5 V (-CD82), and PC3-29 (+CD82) vs. PC3-5 V (-CD82). Top 25 gene lists did not show overlap within the data sets, except (CALB1) the calcium binding protein calbindin 1 which was significantly up-regulated (2.8 log fold change) in PrEC-31 and PC3-29 cells that expressed CD82. Other most significantly up-regulated genes included serine peptidase inhibitor kazal type 1 (SPINK1) and polypeptide N-acetyl galactosaminyl transferase 14 (GALNT14) and most down-regulated genes included C-X-C motif chemokine ligand 14 (CXCL14), urotensin 2 (UTS2D), and fibroblast growth factor 13 (FGF13). Pathways related with cell proliferation and angiogenesis, migration and invasion, cell death, cell cycle, signal transduction, and metabolism were highly enriched in cells that lack CD82 expression. Expression of two mutually inclusive genes in top 100 gene lists of all data sets, runt-related transcription factor (RUNX3) and trefoil factor 3 (TFF3), could be validated with qRT-PCR.

conclusionIdentification of genes and pathways regulated by CD82 in this study may provide additional insights into the role that CD82 plays in prostate tumor progression and metastasis, as well as identify potential targets for therapeutic intervention.

Indexed as

AdenocarcinomaCell Line, TumorGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene OntologyHumansKangai-1 ProteinMaleNeoplasm ProteinsProstatic NeoplasmsRNA InterferenceRNA, Small InterferingTissue Array AnalysisCD82 protein, humanKangai-1 ProteinNeoplasm ProteinsRNA, Small InterferingCD82Gene expressionKAI1Metastasis tumor suppressorMicroarrayProstate cancer

Identifiers

PMID33298014
PMCPMC7724878
OpenAlexW3111411008

What OpenQuestion holds

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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.