Evidence map›Paper›PMID 25220418›Full record

ArticleOncogene2015

SATB2 enhances migration and invasion in osteosarcoma by regulating genes involved in cytoskeletal organization.

B K A Seong, J Lau, T Adderley, L Kee, D Chaukos, M Pienkowska, D Malkin, P Thorner, M S Irwin

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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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 1 institution in 1 country.

B K A Seong1] Departments of Pediatrics and Medical Biophysics, University of Toronto, Toronto, Ontario, Canada [2] Cell Biology Program, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada.
J LauCell Biology Program, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada.
T AdderleyCell Biology Program, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada.
L KeeCell Biology Program, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada.
D ChaukosCell Biology Program, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada.
M PienkowskaProgram in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada.
D Malkin1] Departments of Pediatrics and Medical Biophysics, University of Toronto, Toronto, Ontario, Canada [2] Program in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada [3] Division of Hematology-Oncology, Department of Pediatrics, Hospital for Sick Children, Toronto, Ontario, Canada.
P Thorner1] Department of Pediatric Laboratory Medicine, Hospital for Sick Children, Toronto, Ontario, Canada [2] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
M S Irwin1] Departments of Pediatrics and Medical Biophysics, University of Toronto, Toronto, Ontario, Canada [2] Cell Biology Program, Hospital for Sick Children Research Institute, Peter Gilgan Centre for Research and Learning, Toronto, Ontario, Canada [3] Division of Hematology-Oncology, Department of Pediatrics, Hospital for Sick Children, Toronto, Ontario, Canada [4] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Hospital for Sick Children · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) is the most common malignant bone tumor and the majority of recurrences are due to metastasis. However, the molecular mechanisms that regulate OS metastatic spread are largely unknown. In this study, we report that special AT-rich-binding protein 2 (SATB2) is highly expressed in OS cells and tumors. Short hairpin RNA-mediated knockdown of SATB2 (sh-SATB2) decreases migration and invasion of OS cells without affecting proliferation or viability. Microarray analysis identified genes that were differentially regulated by SATB2 including the actin-binding protein Epithelial Protein Lost In Neoplasm (EPLIN), which was upregulated in sh-SATB2 cells. Silencing EPLIN rescues the decreased invasion observed in sh-SATB2 cells. Pathway analyses of SATB2-regulated genes revealed enrichment of those involved in cytoskeleton dynamics, and increased stress fiber formation was detected in cells with SATB2 knockdown. Furthermore, sh-SATB2 cells exhibit increased RhoA, decreased Rac1 and increased phosphorylation of focal adhesion kinase (FAK) and paxillin. These findings identify SATB2 as a novel regulator of OS invasion, in part via effects on EPLIN and the cytoskeleton.

Indexed as

AnimalsBone NeoplasmsCell MovementCytoskeletal ProteinsCytoskeletonGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMatrix Attachment Region Binding ProteinsMiceMicroarray AnalysisNeoplasm InvasivenessOsteosarcomaTranscription FactorsTumor Cells, CulturedCytoskeletal ProteinsLIMA1 protein, humanMatrix Attachment Region Binding ProteinsSATB2 protein, humanTranscription Factors

Identifiers

PMID25220418
OpenAlexW2041043497

What OpenQuestion holds

Textmetadata
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.