Evidence map›Paper›PMID 25400509›Full record

ArticleCancer cell international2014

The effects of phenoxodiol on the cell cycle of prostate cancer cell lines.

Simon Mahoney, Frank Arfuso, Michael Millward, Arun Dharmarajan

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Triggering of eryptosis, the suicidal erythrocyte death, by phenoxodiol.Naunyn-Schmiedeberg's archives of pharmacology · 2019
    Article
  6. Article
  7. Article
  8. Anti-proliferative Effects ofJournal of cancer prevention · 2017
    Article
  9. 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 2 institutions in 1 country.

Simon MahoneySchool of Anatomy, Physiology and Human Biology, Faculty of Science, The University of Western Australia, Crawley, Perth, WA 6009 Australia.
Frank ArfusoSchool of Anatomy, Physiology and Human Biology, Faculty of Science, The University of Western Australia, Crawley, Perth, WA 6009 Australia ; Curtin Health Innovation Research Institute, Biosciences Research Precinct, School of Biomedical Sciences, Faculty of Health Sciences, Curtin University, GPO Box U1987, 6845 Perth, WA Australia.
Michael MillwardSchool of Medicine and Pharmacology, The University of Western Australia, Crawley, Perth, WA 6009 Australia.
Arun DharmarajanSchool of Anatomy, Physiology and Human Biology, Faculty of Science, The University of Western Australia, Crawley, Perth, WA 6009 Australia ; Curtin Health Innovation Research Institute, Biosciences Research Precinct, School of Biomedical Sciences, Faculty of Health Sciences, Curtin University, GPO Box U1987, 6845 Perth, WA Australia.
University of Western Australia · AUCurtin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of the isoflavone phenoxodiol on the expression of cell cycle genes.

methodsThree prostate cancer cell lines-LNCaP, DU145, and PC3 were cultured in vitro, and then treated with phenoxodiol (10 μM and 30 μM) for 24 and 48 h. The expression of cell cycle genes p21(WAF1), c-Myc, Cyclin-D1, and Ki-67 was investigated by Real Time PCR.

resultsHere we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21(WAF1) in all the cell lines in response to treatment, indicating that activation of p21(WAF1) and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation. We found that c-Myc and Cyclin-D1 expression was not consistently altered across all cell lines but Ki-67 signalling expression was decreased in line with the cell cycle arrest.

conclusionsPhenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21(WAF1) and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions. These data indicate that phenoxodiol would be effective as a potential future treatment modality for both hormone sensitive and hormone refractory prostate cancer.

Indexed as

Cell cycleCytotoxicityPhenoxodiolProstate cancer

Identifiers

PMID25400509
PMCPMC4231195
OpenAlexW2116160307

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.