Evidence map›Paper›PMID 22737267›Full record

ArticleGenes & cancer2011

Maspin reprograms the gene expression profile of prostate carcinoma cells for differentiation.

M Margarida Bernardo, Yonghong Meng, Jaron Lockett, Gregory Dyson, Alan Dombkowski, Alexander Kaplun, Xiaohua Li, Shuping Yin, Sijana Dzinic, Mary Olive and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Genes & cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. An Essential Role ofCancer research · 2017
    Article
  14. Article
  15. Article
  16. Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  17. Article
  18. Tumor suppressor maspin as a modulator of host immune response to cancer.Bosnian journal of basic medical sciences · 2015
    Review
  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

17 authors at 3 institutions in 1 country.

M Margarida BernardoWayne State University School of Medicine, Detroit, MI, USA.
Yonghong Meng
Jaron Lockett
Gregory Dyson
Alan Dombkowski
Alexander Kaplun
Xiaohua Li
Shuping Yin
Sijana Dzinic
Mary Olive
Ivory Dean
David Krass
Kamiar Moin
R Daniel Bonfil
Michael Cher
Wael Sakr
Shijie Sheng
Wayne State University · USNational Institutes of Health · USUniversity of California, Los Angeles · US

Funding

The therapeutic potential of maspin in prostate cancerR01CA084176 · NCI · WAYNE STATE UNIVERSITY · PI SHENG, SHIJIE · 2001 to 2011
$2.7M
A Role of Novel Serpin Maspinin Prostate Tumor/Bone InteractionR01CA127735 · NCI · WAYNE STATE UNIVERSITY · PI SHENG, SHIJIE · 2008 to 2012
$1.5M
NCI NIH HHS R01 CA084176NCI NIH HHS R01 CA127735
6 · The paper itself

Abstract

Maspin is an epithelial-specific tumor suppressor gene. Previous data suggest that maspin expression may redirect poorly differentiated tumor cells to better differentiated phenotypes. Further, maspin is the first and only endogenous polypeptide inhibitor of histone deacetylase 1 (HDAC1) identified thus far. In the current study, to address what central program of tumor cell redifferentiation is regulated by maspin and how tumor microenvironments further define the effects of maspin, we conducted a systematic and extensive comparison of prostate tumor cells grown in 2-dimensional culture, in 3-dimensional collagen I culture, and as in vivo bone tumors. We showed that maspin was sufficient to drive prostate tumor cells through a spectrum of temporally and spatially polarized cellular processes of redifferentiation, a reversal of epithelial-to-mesenchymal transition (EMT). Genes commonly regulated by maspin were a small subset of HDAC target genes that are closely associated with epithelial differentiation and TGFβ signaling. These results suggest that a specific endogenous HDAC inhibitor may regulate one functionally related subset of HDAC target genes, although additional maspin-induced changes of gene expression may result from tumor interaction with its specific microenvironments. Currently, EMT is recognized as a critical step in tumor progression. To this end, our current study uncovered a link between maspin and a specific mechanism of prostate epithelial differentiation that can reverse EMT.

Indexed as

cell differentiationmicroarray analysisorganotypic model

Identifiers

PMID22737267
PMCPMC3379563
OpenAlexW2123715172

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.