Evidence map›Paper›PMID 26643866›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2016

HDAC6 activity is not required for basal autophagic flux in metastatic prostate cancer cells.

Gregory W Watson, Samanthi Wickramasekara, Yufeng Fang, Claudia S Maier, David E Williams, Roderick H Dashwood, Viviana I Perez, Emily Ho

Abstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Zinc deficiency alters the susceptibility of pancreatic beta cells (INS-1) to arsenic exposure.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2019
    Article
  5. Article
  6. Article
  7. 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

8 authors at 3 institutions in 1 country.

Gregory W WatsonMolecular and Cellular Biology Program, Oregon State University, Corvallis, OR 97331, USA Biological and Population Health Sciences, Oregon State University, Corvallis, OR 97331, USA.
Samanthi WickramasekaraDepartment of Chemistry, Oregon State University, Corvallis, OR 97331, USA.
Yufeng FangGenetics, Bioinformatics & Computational Biology, Virginia Tech, Blacksburg, VA 24061, USA.
Claudia S MaierDepartment of Chemistry, Oregon State University, Corvallis, OR 97331, USA.
David E WilliamsEnvironmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
Roderick H DashwoodCenter for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M Science Center, Houston, TX 77030, USA Department of Nutrition & Food Science, Texas A&M University, College Station, TX 77030, USA Department of Clinical Cancer Prevention, MD Anderson Cancer Center, Houston, TX 77030, USA Department of Molecular & Cellular Medicine, Texas A&M University College of Medicine, College Station, TX 77030, USA.
Viviana I PerezLinus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA Department of Biochemistry and Biophysics, Oregon State University, Corvallis, OR 97331, USA.
Emily HoBiological and Population Health Sciences, Oregon State University, Corvallis, OR 97331, USA Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA emily.ho@oregonstate.edu.
Oregon State University · USThe University of Texas MD Anderson Cancer Center · USVirginia Tech · 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

Histone deacetylase 6 is a multifunctional lysine deacetylase that is recently emerging as a central facilitator of response to stress and may play an important role in cancer cell proliferation. The histone deacetylase 6-inhibitor tubacin has been shown to slow the growth of metastatic prostate cancer cells and sensitize cancer cells to chemotherapeutic agents. However, the proteins histone deacetylase 6 interacts with, and thus its role in cancer cells, remains poorly characterized. Histone deacetylase 6 deacetylase activity has recently been shown to be required for efficient basal autophagic flux. Autophagy is often dysregulated in cancer cells and may confer stress resistance and allow for cell maintenance and a high proliferation rate. Tubacin may therefore slow cancer cell proliferation by decreasing autophagic flux. We characterized the histone deacetylase 6-interacting proteins in LNCaP metastatic prostate cancer cells and found that histone deacetylase 6 interacts with proteins involved in several cellular processes, including autophagy. Based on our interaction screen, we assessed the impact of the histone deacetylase 6-inhibitor tubacin on autophagic flux in two metastatic prostate cancer cell lines and found that tubacin does not influence autophagic flux. Histone deacetylase 6 therefore influences cell proliferation through an autophagy-independent mechanism.

Indexed as

AutophagyCell Line, TumorCell ProliferationHistone Deacetylase 6Histone DeacetylasesHumansMaleProtein Interaction MappingHDAC6 protein, humanHistone Deacetylase 6Histone DeacetylasesAutophagyHDAC6metastatic prostate cancertubacin

Identifiers

PMID26643866
PMCPMC4950308
OpenAlexW2328880451

What OpenQuestion holds

Textmetadata
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.