Evidence map›Paper›PMID 17668048›Full record

ArticlePloS one2007

p53 target gene SMAR1 is dysregulated in breast cancer: its role in cancer cell migration and invasion.

Kamini Singh, Devraj Mogare, Ramprasad Obula Giridharagopalan, Rajinikanth Gogiraju, Gopal Pande, Samit Chattopadhyay

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Oncotarget · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Bridged Analogues for p53-Dependent Cancer Therapy Obtained by S-Alkylation.International journal of peptide research and therapeutics · 2016
    Article
  15. Article
  16. Nuclear matrix-associated protein SMAR1 regulates alternative splicing via HDAC6-mediated deacetylation of Sam68.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Kamini SinghNational Centre for Cell Science, Pune University, Pune, Maharastra, India.
Devraj Mogare
Ramprasad Obula Giridharagopalan
Rajinikanth Gogiraju
Gopal Pande
Samit Chattopadhyay
Centre for Cellular and Molecular Biology · INNational Centre for Cell Science · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor suppressor SMAR1 interacts and stabilizes p53 through phosphorylation at its serine-15 residue. We show that SMAR1 transcription is regulated by p53 through its response element present in the SMAR1 promoter. Upon Doxorubicin induced DNA damage, acetylated p53 is recruited on SMAR1 promoter that allows activation of its transcription. Once SMAR1 is induced, cell cycle arrest is observed that is correlated to increased phospho-ser-15-p53 and decreased p53 acetylation. Further we demonstrate that SMAR1 expression is drastically reduced during advancement of human breast cancer. This was correlated with defective p53 expression in breast cancer where acetylated p53 is sequestered into the heterochromatin region and become inaccessible to activate SMAR1 promoter. In a recent report we have shown that SMAR1 represses Cyclin D1 transcription through recruitment of HDAC1 dependent repressor complex at the MAR site of Cyclin D1 promoter. Here we show that downmodulation of SMAR1 in high grade breast carcinoma is correlated with upregulated Cyclin D1 expression. We also established that SMAR1 inhibits tumor cell migration and metastases through inhibition of TGFbeta signaling and its downstream target genes including cutl1 and various focal adhesion molecules. Thus, we report that SMAR1 plays a central role in coordinating p53 and TGFbeta pathways in human breast cancer.

Indexed as

Breast NeoplasmsCell CycleCell Cycle ProteinsCell MovementCell NucleusCytoplasmDNA-Binding ProteinsDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsNeoplasm StagingNuclear ProteinsBANP protein, humanCell Cycle ProteinsDNA-Binding ProteinsNeoplasm ProteinsNuclear ProteinsTransforming Growth Factor betaTumor Suppressor Protein p53

Identifiers

PMID17668048
PMCPMC1924604
OpenAlexW2015872419

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.