Evidence map›Paper›PMID 19284555›Full record

ArticleMolecular cancer2009

delta-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profiles.

Yan Zeng, Agustin Abdallah, Jian-Ping Lu, Tao Wang, Yan-Hua Chen, David M Terrian, Kwonseop Kim, Qun Lu

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  4. Predicting the germline dependence of hematuria risk in prostate cancer radiotherapy patients.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023
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  7. δ-Catenin Participates in EGF/AKT/p21International journal of molecular sciences · 2021
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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 3 institutions in 3 countries.

Yan ZengDepartment of Anatomy and Cell Biology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA. zy717@yeah.net
Agustin Abdallah
Jian-Ping Lu
Tao Wang
Yan-Hua Chen
David M Terrian
Kwonseop Kim
Qun Lu
East Carolina University · USCapital Medical University · CNChonnam National University · KR

Funding

delta-Catenin and Cell-Cell Adhesion in Prostate CancerR01CA111891 · NCI · EAST CAROLINA UNIVERSITY · PI LU, QUN · 2006 to 2010
$759k
NCI NIH HHS CA111891NCI NIH HHS R01 CA111891
6 · The paper itself

Abstract

backgrounddelta-Catenin is a unique member of beta-catenin/armadillo domain superfamily proteins and its primary expression is restricted to the brain. However, delta-catenin is upregulated in human prostatic adenocarcinomas, although the effects of delta-catenin overexpression in prostate cancer are unclear. We hypothesized that delta-catenin plays a direct role in prostate cancer progression by altering gene profiles of cell cycle regulation and cell survival.

resultsWe employed gene transfection and small interfering RNA to demonstrate that increased delta-catenin expression promoted, whereas its knockdown suppressed prostate cancer cell viability. delta-Catenin promoted prostate cancer cell colony formation in soft agar as well as tumor xenograft growth in nude mice. Deletion of either the amino-terminal or carboxyl-terminal sequences outside the armadillo domains abolished the tumor promoting effects of delta-catenin. Quantitative RT2 Profiler PCR Arrays demonstrated gene alterations involved in cell cycle and survival regulation. delta-Catenin overexpression upregulated cyclin D1 and cdc34, increased phosphorylated histone-H3, and promoted the entry of mitosis. In addition, delta-catenin overexpression resulted in increased expression of cell survival genes Bcl-2 and survivin while reducing the cell cycle inhibitor p21Cip1.

conclusionTaken together, our studies suggest that at least one consequence of an increased expression of delta-catenin in human prostate cancer is the alteration of cell cycle and survival gene profiles, thereby promoting tumor progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsArmadillo Domain ProteinsCateninsCell AdhesionCell Adhesion MoleculesCell CycleCell ProliferationCell SurvivalDelta CateninDisease ProgressionMaleMiceMice, NudeMitosisPhosphoproteinsArmadillo Domain ProteinsCateninsCell Adhesion MoleculesDelta CateninPhosphoproteins

Identifiers

PMID19284555
PMCPMC2660279
OpenAlexW1967784918

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.