Evidence map›Paper›PMID 10393844›Full record

ArticleThe American journal of pathology1999

Suppression of prostate carcinoma cell invasion by expression of antisense L-plastin gene.

J Zheng, N Rudra-Ganguly, W C Powell, P Roy-Burman

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Meta-analysis of oncogenic protein kinase Ciota signaling in lung adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Discovering functional relationships between RNA expression and chemotherapeutic susceptibility using relevance networks.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  16. 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

4 authors at 1 institution in 1 country.

J ZhengDepartments of Pathology, University of Southern California School of Medicine, Los Angeles, California, USA.
N Rudra-Ganguly
W C Powell
P Roy-Burman
University of Southern California · US

Funding

PATHOGENESIS OF HUMAN PROSTATE CARCINOMASR01CA059705 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROY-BURMAN, PRADIP · 1993 to 2012
$7.3M
VIRAL AND CHEMICAL CARCINOGENESIST32CA009320 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 1985 to 2012
$2.5M
VIROLOGY, IMMUNOLOGY &ONCOLOGY: MECHANISMS OF DISEASET32AI007078 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LAI, MICHAEL M.C. · 1985 to 2006
$1.1M
NCI NIH HHS CA-59705NCI NIH HHS R01 CA059705NCI NIH HHS T32 CA009320NCI NIH HHS T32-CA09320NIAID NIH HHS T32 AI007078NIAID NIH HHS T32-AI07078
6 · The paper itself

Abstract

Based on the finding that gene expression for the actin-bundling protein L-plastin is inducible by androgen and that L-plastin is overexpressed in malignant epithelium of the prostate, we examined the functional consequences of L-plastin down-regulation in prostate carcinoma cell lines by both transfection and retroviral infection. We constructed retroviral vectors to express two different regions of the L-plastin gene, a 1713-bp 3'-coding portion and a 163-bp 5'-untranslated region, both in antisense orientation. Introduction of either constructs into prostate carcinoma cell lines, PC-3 and its isogenic but metastatic variant PC-3M cells, reduced the growth rates of both cell lines. In vitro invasion and motility of PC-3 and PC-3M cells were drastically suppressed (approximately 10-fold) by the expression of the antisense constructs. Evidence was obtained to indicate that L-plastin protein levels were indeed decreased by the antisense expression. The antisense construct for the 5'-untranslated region with the most unique sequence for the L-plastin gene was more effective in down-regulation efficiency compared with the larger antisense construct in the coding region, which maintains homology to other members of the plastin gene family. Cells infected with the 163-bp antisense virus, which were also tested in a nude mouse diaphragm invasion model, showed suppression of in vivo invasion of both PC-3 and PC-3M cells. These results suggested that overexpression of L-plastin might be functionally involved in prostate cancer invasion and metastasis, and raised the possibility that L-plastin gene-specific antisense delivery could potentially be a useful approach to interfere with prostate cancer progression in vivo.

Indexed as

AnimalsAntisense Elements (Genetics)CarcinomaCell DivisionCell MovementMaleMembrane GlycoproteinsMiceMice, NudeMicrofilament ProteinsNeoplasm InvasivenessPhosphoproteinsProstatic NeoplasmsAntisense Elements (Genetics)Membrane GlycoproteinsMicrofilament ProteinsPhosphoproteinsplastin

Identifiers

PMID10393844
PMCPMC1866644
OpenAlexW2006058936

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.