Evidence map›Paper›PMID 26739564›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

SDPR functions as a metastasis suppressor in breast cancer by promoting apoptosis.

Sait Ozturk, Panagiotis Papageorgis, Chen Khuan Wong, Arthur W Lambert, Hamid M Abdolmaleky, Arunthathi Thiagalingam, Herbert T Cohen, Sam Thiagalingam

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

8 authors at 1 institution in 1 country.

Sait OzturkCell and Molecular Biology Graduate Program, Boston University School of Medicine, Boston, MA 02118; Molecular and Translational Medicine Graduate Program, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Biomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118;
Panagiotis PapageorgisBiomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Genetics and Genomics Graduate Program, Boston University School of Medicine, Boston, MA 02118;
Chen Khuan WongBiomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Genetics and Genomics Graduate Program, Boston University School of Medicine, Boston, MA 02118;
Arthur W LambertMolecular and Translational Medicine Graduate Program, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Biomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118;
Hamid M AbdolmalekyBiomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118;
Arunthathi ThiagalingamBiomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118;
Herbert T CohenCell and Molecular Biology Graduate Program, Boston University School of Medicine, Boston, MA 02118; Molecular and Translational Medicine Graduate Program, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118.
Sam ThiagalingamCell and Molecular Biology Graduate Program, Boston University School of Medicine, Boston, MA 02118; Molecular and Translational Medicine Graduate Program, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Biomedical Genetics Section and Cancer Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Genetics and Genomics Graduate Program, Boston University School of Medicine, Boston, MA 02118; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118 samthia@bu.edu.
Boston University · US

Funding

Boston University Clinical and Translational Science Award (CTSA) Program UL1UL1TR000157 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2012 to 2013
$7.9M
The role of hBUB1-p53 pathway in genomic stability.R01CA101773 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI THIAGALINGAM, SAM · 2003 to 2007
$1.5M
Genetic Determinants of Epithelial DNA Damage in SmokersR01ES010377 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI THIAGALINGAM, SAM · 2001 to 2004
$1.5M
Dissecting the metastasis suppressor complex to identify colon cancer biomarkersR21CA165707 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI THIAGALINGAM, SAM · 2013 to 2014
$386k
NCATS NIH HHS UL1 TR000157NCATS NIH HHS UL1-TR000157NCI NIH HHS CA165707NCI NIH HHS R01 CA101773NCI NIH HHS R21 CA165707NIEHS NIH HHS R01 ES010377
6 · The paper itself

Abstract

Metastatic dissemination of breast cancer cells represents a significant clinical obstacle to curative therapy. The loss of function of metastasis suppressor genes is a major rate-limiting step in breast cancer progression that prevents the formation of new colonies at distal sites. However, the discovery of new metastasis suppressor genes in breast cancer using genomic efforts has been slow, potentially due to their primary regulation by epigenetic mechanisms. Here, we report the use of model cell lines with the same genetic lineage for the identification of a novel metastasis suppressor gene, serum deprivation response (SDPR), localized to 2q32-33, a region reported to be associated with significant loss of heterozygosity in breast cancer. In silico metaanalysis of publicly available gene expression datasets suggests that the loss of expression of SDPR correlates with significantly reduced distant-metastasis-free and relapse-free survival of breast cancer patients who underwent therapy. Furthermore, we found that stable SDPR overexpression in highly metastatic breast cancer model cell lines inhibited prosurvival pathways, shifted the balance of Bcl-2 family proteins in favor of apoptosis, and decreased migration and intravasation/extravasation potential, with a corresponding drastic suppression of metastatic nodule formation in the lungs of NOD/SCID mice. Moreover, SDPR expression is silenced by promoter DNA methylation, and as such it exemplifies epigenetic regulation of metastatic breast cancer progression. These observations highlight SDPR as a potential prognostic biomarker and a target for future therapeutic applications.

Indexed as

ApoptosisAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorCell MovementDisease ProgressionDown-RegulationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMice, Inbred NODPhosphate-Binding ProteinsCarrier ProteinsCAVIN2 protein, humanPhosphate-Binding Proteinsbreast cancerepigeneticsmetastasismetastasis suppressorSDPR

Identifiers

PMID26739564
PMCPMC4725521
OpenAlexW2231768726

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.