Evidence map›Paper›PMID 20466611›Full record

ArticleCancer epidemiology2010

Cholesterol and phytosterols differentially regulate the expression of caveolin 1 and a downstream prostate cell growth-suppressor gene.

Godwin O Ifere, Anita Equan, Kereen Gordon, Peri Nagappan, Joseph U Igietseme, Godwin A Ananaba

Open access · greenAbstract read
In one paragraph

Article in Cancer epidemiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Mechanism of inhibition of Shiga-toxigenicCell death discovery · 2018
    Article
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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

6 authors at 2 institutions in 1 country.

Godwin O IfereDepartment of Biological Sciences, Clark Atlanta University, Atlanta, GA 30314, USA. gifere@cau.edu
Anita Equan
Kereen Gordon
Peri Nagappan
Joseph U Igietseme
Godwin A Ananaba
Clark Atlanta University · USCenters for Disease Control and Prevention · US

Funding

THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
VIRTUAL REALITY TECHNOLOGY IN TREATMENT OF FEARS AND PHOBIASS06GM008247 · NIGMS · CLARK ATLANTA UNIVERSITY · PI KHAN, ISHRAT M · 1989 to 2008
$6.6M
NCRR NIH HHS G12 RR003062NCRR NIH HHS G12RR003062NIGMS NIH HHS GM08247NIGMS NIH HHS S06 GM008247PHS HHS A141231
6 · The paper itself

Abstract

backgroundThe purpose of our study was to show the distinction between the apoptotic and anti-proliferative signaling of phytosterols and cholesterol-enrichment in prostate cancer cell lines, mediated by the differential transcription of caveolin-1, and N-myc downstream-regulated gene 1 (NDRG1), a pro-apoptotic androgen-regulated tumor suppressor.

methodsPC-3 and DU145 cells were treated with sterols (cholesterol and phytosterols) for 72h, followed by trypan blue dye-exclusion measurement of necrosis and cell growth measured with a Coulter counter. Sterol induction of cell growth-suppressor gene expression was evaluated by mRNA transcription using RT-PCR, while cell cycle analysis was performed by FACS analysis. Altered expression of Ndrg1 protein was confirmed by Western blot analysis. Apoptosis was evaluated by real time RT-PCR amplification of P53, Bcl-2 gene and its related pro- and anti-apoptotic family members.

resultsPhysiological doses (16microM) of cholesterol and phytosterols were not cytotoxic in these cells. Cholesterol-enrichment promoted cell growth (P<0.05), while phytosterols significantly induced growth-suppression (P<0.05) and apoptosis. Cell cycle analysis showed that contrary to cholesterol, phytosterols decreased mitotic subpopulations. We demonstrated for the first time that cholesterols concertedly attenuated the expression of caveolin-1 (cav-1) and NDRG1 genes in both prostate cancer cell lines. Phytosterols had the opposite effect by inducing overexpression of cav-1, a known mediator of androgen-dependent signals that presumably control cell growth or apoptosis.

conclusionsCholesterol and phytosterol treatment differentially regulated the growth of prostate cancer cells and the expression of p53 and cav-1, a gene that regulates androgen-regulated signals. These sterols also differentially regulated cell cycle arrest, downstream pro-apoptotic androgen-regulated tumor suppressor, NDRG1 suggesting that cav-1 may mediate pro-apoptotic NDRG1 signals. Elucidation of the mechanism for sterol modulation of growth and apoptosis signaling may reveal potential targets for cancer prevention and/or chemotherapeutic intervention. Sterol regulation of NDRG1 transcription suggests its potential as biomarker for prediction of neoplasms that would be responsive to chemoprevention by phytosterols.

Indexed as

ApoptosisBlotting, WesternCaveolin 1Cell Cycle ProteinsCell ProliferationCholesterolFlow CytometryGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMaleN-myc Downstream-Regulated Gene 1 ProteinPhytosterolsProstatic NeoplasmsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerCAV1 protein, humanCaveolin 1Cell Cycle ProteinsCholesterolIntracellular Signaling Peptides and ProteinsN-myc Downstream-Regulated Gene 1 ProteinPhytosterolsRNA, Messenger

Identifiers

PMID20466611
PMCPMC2939726
OpenAlexW2147692954

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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.