Evidence map›Paper›PMID 25486523›Full record

ArticleOncogenesis2014

SUV39H1/H3K9me3 attenuates sulforaphane-induced apoptotic signaling in PC3 prostate cancer cells.

G W Watson, S Wickramasekara, Z Palomera-Sanchez, C Black, C S Maier, D E Williams, R H Dashwood, E Ho

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 28 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

8 authors at 1 institution in 1 country.

G W Watson1] Department of Molecular and Cellular Biology, Oregon State University, Corvallis, OR, USA [2] College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA.
S WickramasekaraDepartment of Chemistry, Oregon State University, Corvallis, OR, USA.
Z Palomera-SanchezCollege of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA.
C BlackCollege of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA.
C S MaierDepartment of Chemistry, Oregon State University, Corvallis, OR, USA.
D E Williams1] Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR, USA [2] Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
R H Dashwood1] Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR, USA [2] Center for Epigenetics and Disease Prevention, Texas A&M Health Science Center, Houston, TX, USA.
E Ho1] Department of Molecular and Cellular Biology, Oregon State University, Corvallis, OR, USA [2] College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA [3] Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
Oregon State University · US

Funding

Reducing Susceptibility to Environmental Stress Throughout the Life SpanP30ES000210 · NIEHS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 1985 to 2015
$21.4M
Transplacental Chemoprevention of Lung Tumors and LymphomasP01CA090890 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI DASHWOOD, RODERICK H · 2003 to 2014
$14.2M
NCI NIH HHS P01 CA090890NIEHS NIH HHS P30 ES000210
6 · The paper itself

Abstract

The isothiocyanate sulforaphane is a promising molecule for development as a therapeutic agent for patients with metastatic prostate cancer. Sulforaphane induces apoptosis in advanced prostate cancer cells, slows disease progression in vivo and is well tolerated at pharmacological doses. However, the underlying mechanism(s) responsible for cancer suppression remain to be fully elucidated. In this investigation we demonstrate that sulforaphane induces posttranslational modification of histone methyltransferase SUV39H1 in metastatic, androgen receptor-negative PC3 prostate cancer cells. Sulforaphane stimulates ubiquitination and acetylation of SUV39H1 within a C-terminal nuclear localization signal peptide motif and coincides with its dissociation from chromatin and a decrease in global trimethyl-histone H3 lysine 9 (H3K9me3) levels. Exogenous SUV39H1 expression leads to an increase in H3K9me3 and decreases sulforaphane-induced apoptotic signaling. SUV39H1 is thus identified as a novel mediator of sulforaphane cytotoxicity in PC3 cells. Our results also suggest SUV39H1 dynamics as a new therapeutic target in advanced prostate cancers.

Identifiers

PMID25486523
PMCPMC4275561
OpenAlexW2054933678

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.