Evidence map›Paper›PMID 28615627›Full record

ArticleScientific reports2017

Reduction in Migratory Phenotype in a Metastasized Breast Cancer Cell Line via Downregulation of S100A4 and GRM3.

Andy Chen, Luqi Wang, Bai-Yan Li, Jesse Sherman, Jong E Ryu, Kazunori Hamamura, Yunlong Liu, Harikrishna Nakshatri, Hiroki Yokota

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  6. Epigenetic reprogramming in cancer: From diagnosis to treatment.Frontiers in cell and developmental biology · 2023
    Review
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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

9 authors at 6 institutions in 3 countries.

Andy ChenWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, 47907, USA.
Luqi WangDepartment of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN, 46202, USA.
Bai-Yan LiDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, 150081, China.
Jesse ShermanDepartment of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN, 46202, USA.
Jong E RyuDepartment of Mechanical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN, 46202, USA.
Kazunori HamamuraDepartment of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya, Japan.
Yunlong LiuDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Harikrishna NakshatriDepartment of Surgery, Simon Cancer Research Center, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Hiroki YokotaDepartment of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN, 46202, USA. hyokota@iupui.edu.
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineAichi Gakuin University · JPHarbin Medical University · CNPurdue University West Lafayette · USUniversity of Indianapolis · US

Funding

Boston University Clinical and Translational Science Institute - U ProgramU54TR001012 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2014 to 2014
$3.9M
NCATS NIH HHS U54 TR001012
6 · The paper itself

Abstract

To investigate phenotypic and genotypic alterations before and after bone metastasis, we conducted genome-wide mRNA profiling and DNA exon sequencing of two cell lines (TMD and BMD) derived from a mouse xenograft model. TMD cells were harvested from the mammary fat pad after transfecting MDA-MB-231 breast cancer cells, while BMD cells were isolated from the metastasized bone. Compared to BMD cells, TMD cells exhibited higher cellular motility. In contrast, BMD cells formed a spheroid with a smoother and more circular surface when co-cultured with osteoblasts. In characterizing mRNA expression using principal component analysis, S100 calcium-binding protein A4 (S100A4) was aligned to a principal axis associated with metastasis. Partial silencing of S100A4 suppressed migratory capabilities of TMD cells, while Paclitaxel decreased the S100A4 level and reduced TMD's cellular motility. DNA mutation analysis revealed that the glutamate metabotropic receptor 3 (GRM3) gene gained a premature stop codon in BMD cells, and silencing GRM3 in TMD cells altered their spheroid shape closer to that of BMD cells. Collectively, this study demonstrates that metastasized cells are less migratory due in part to the post-metastatic downregulation of S100A4 and GRM3. Targeting S100A4 and GRM3 may help prevent bone metastasis.

Indexed as

Gene Expression Regulation, Neoplastic3',5'-Cyclic-AMP PhosphodiesterasesCell Line, TumorCell MovementGenome-Wide Association StudyHumansIntegrin beta ChainsMatrix Metalloproteinase 9MutationPhenotypeReceptors, Metabotropic GlutamateRNA InterferenceRNA, Small InterferingS100 Calcium-Binding Protein A43',5'-Cyclic-AMP PhosphodiesterasesIntegrin beta ChainsMatrix Metalloproteinase 9Receptors, Metabotropic GlutamateRNA, Small InterferingS100A4 protein, humanS100 Calcium-Binding Protein A4

Identifiers

PMID28615627
PMCPMC5471271
OpenAlexW2622329638

What OpenQuestion holds

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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.