Evidence map›Paper›PMID 17909025›Full record

ArticleCancer research2007

Roles for the stem cell associated intermediate filament Nestin in prostate cancer migration and metastasis.

Wolfram Kleeberger, G Steven Bova, Matthew E Nielsen, Mehsati Herawi, Ai-Ying Chuang, Jonathan I Epstein, David M Berman

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 1 pooled it
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

92 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Distribution, contribution and regulation of nestinJournal of advanced research · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Emerging biomarker in carcinogenesis. Focus on Nestin.Postepy dermatologii i alergologii · 2022
    Review
  13. Androgens, aging, and prostate health.Reviews in endocrine & metabolic disorders · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

32 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Wolfram KleebergerDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.
G Steven Bova
Matthew E Nielsen
Mehsati Herawi
Ai-Ying Chuang
Jonathan I Epstein
David M Berman
Neurology, Inc · USJohns Hopkins Medicine · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA058236NCI NIH HHS P50 CA58236NIDDK NIH HHS DK05937
6 · The paper itself

Abstract

The intermediate filament protein Nestin identifies stem/progenitor cells in adult tissues, but the function of Nestin is poorly understood. We investigated Nestin expression and function in common lethal cancers. Nestin mRNA was detected in cell lines from small cell lung, and breast cancers, and particularly elevated in cell lines derived from prostate cancer metastases. Whereas the androgen-independent lines PC3, 22RV1, and DU145 all expressed Nestin transcripts under standard culture conditions, the androgen-dependent line LnCaP expressed Nestin only on androgen withdrawal. We confirmed associations of Nestin expression, androgen withdrawal, and metastatic potential by immunohistochemical analysis of samples from 254 prostate cancer patients. Cytoplasmic Nestin protein was readily identifiable in prostate cancer cells from 75% of patients with lethal androgen-independent disease, even in cancer sampled from the prostate itself. However, Nestin expression was undetectable in localized androgen-deprived tumors and in metastases without prior androgen deprivation. To address its function, we reduced Nestin levels with short hairpin RNAs, markedly inhibiting in vitro migration and invasion in prostate cancer cells but leaving cell growth intact. Nestin knockdown also diminished metastases 5-fold compared with controls despite uncompromised tumorigenicity at the site of inoculation. These results specify a function for Nestin in cell motility and identify a novel pathway for prostate cancer metastasis. Activity of this pathway may be selected by the extraprostatic environment or, as supported by our data, may originate within the prostate after androgen deprivation. Further dissection of this novel Nestin migration pathway may lead to strategies to prevent and neutralize metastatic spread.

Indexed as

AnimalsCell Growth ProcessesCell Line, TumorCell MovementFemaleHCT116 CellsHumansImmunohistochemistryIntermediate Filament ProteinsMaleMiceMice, NudeNeoplasm MetastasisNerve Tissue ProteinsNestinProstatic NeoplasmsIntermediate Filament ProteinsNerve Tissue ProteinsNES protein, humanNes protein, mouseNestin

Identifiers

PMID17909025
PMCPMC3072059
OpenAlexW2142453444

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.