Evidence map›Paper›PMID 23785446›Full record

ArticlePloS one2013

Cholestane-3β, 5α, 6β-triol suppresses proliferation, migration, and invasion of human prostate cancer cells.

Ching-Yu Lin, Chieh Huo, Li-Kuo Kuo, Richard A Hiipakka, Richard Baker Jones, Hui-Ping Lin, Yuwen Hung, Liang-Cheng Su, Jen-Chih Tseng, Ying-Yu Kuo and 12 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

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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

22 authors at 7 institutions in 2 countries.

Ching-Yu LinInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.
Chieh Huo
Li-Kuo Kuo
Richard A Hiipakka
Richard Baker Jones
Hui-Ping Lin
Yuwen Hung
Liang-Cheng Su
Jen-Chih Tseng
Ying-Yu Kuo
Yu-Ling Wang
Yasuhisa Fukui
Yung-Hsi Kao
John M Kokontis
Chien-Chih Yeh
Linyi Chen
Shiaw-Der Yang
Hsiao-Hui Fu
Ya-Wen Chen
Kelvin K C Tsai
Jang-Yang Chang
Chih-Pin Chuu
National Health Research Institutes · TWNational Tsing Hua University · TWUniversity of Chicago · USNational Central University · TWChina Medical University · TWMackay Memorial Hospital · TWTaoyuan Armed Forces General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxysterols are oxidation products of cholesterol. Cholestane-3β, 5α, 6β-triol (abbreviated as triol) is one of the most abundant and active oxysterols. Here, we report that triol exhibits anti-cancer activity against human prostate cancer cells. Treatment of cells with triol dose-dependently suppressed proliferation of LNCaP CDXR-3, DU-145, and PC-3 human prostate cancer cells and reduced colony formation in soft agar. Oral administration of triol at 20 mg/kg daily for three weeks significantly retarded the growth of PC-3 xenografts in nude mice. Flow cytometric analysis revealed that triol treatment at 10-40 µM caused G1 cell cycle arrest while the TUNEL assay indicated that triol treatment at 20-40 µM induced apoptosis in all three cell lines. Micro-Western Arrays and traditional Western blotting methods indicated that triol treatment resulted in reduced expression of Akt1, phospho-Akt Ser473, phospho-Akt Thr308, PDK1, c-Myc, and Skp2 protein levels as well as accumulation of the cell cycle inhibitor p27(Kip). Triol treatment also resulted in reduced Akt1 protein expression in PC-3 xenografts. Overexpression of Skp2 in PC-3 cells partially rescued the growth inhibition caused by triol. Triol treatment suppressed migration and invasion of DU-145, PC-3, and CDXR-3 cells. The expression levels of proteins associated with epithelial-mesenchymal transition as well as focal adhesion kinase were affected by triol treatment in these cells. Triol treatment caused increased expression of E-cadherin protein levels but decreased expression of N-cadherin, vimentin, Slug, FAK, phospho-FAK Ser722, and phospho-FAK Tyr861 protein levels. Confocal laser microscopy revealed redistribution of β-actin and α-tubulin at the periphery of the CDXR-3 and DU-145 cells. Our observations suggest that triol may represent a promising therapeutic agent for advanced metastatic prostate cancer.

Indexed as

ActinsAndrogensAnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell MovementCell ProliferationCholestanolsDisease Models, AnimalEpithelial-Mesenchymal TransitionG1 Phase Cell Cycle CheckpointsGene ExpressionHumansLiver X ReceptorsMaleActinsAndrogensAntineoplastic Agentscholestane-3,5,6-triolCholestanolsLiver X ReceptorsOrphan Nuclear ReceptorsProteomeProto-Oncogene Proteins c-aktS-Phase Kinase-Associated ProteinsTubulin

Identifiers

PMID23785446
PMCPMC3681800
OpenAlexW1999839830

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.