Evidence map›Paper›PMID 31865176›Full record

ArticleTranslational oncology2020

Inhibition of HDAC6 Attenuates Tumor Growth of Non-Small Cell Lung Cancer.

Brian Deskin, Qinyan Yin, Yan Zhuang, Shigeki Saito, Bin Shan, Joseph A Lasky

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  20. Histone Deacetylase Inhibition in Non-small Cell Lung Cancer: Hype or Hope?Frontiers in cell and developmental biology · 2020
    Review
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 3 institutions in 1 country.

Brian DeskinTulane University Health Sciences Center, Department of Medicine, New Orleans, LA 70112, USA; Epigenetics & Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: bdeskin@hsph.harvard.edu.
Qinyan YinTulane University Health Sciences Center, Department of Medicine, New Orleans, LA 70112, USA.
Yan ZhuangTulane University Health Sciences Center, Department of Medicine, New Orleans, LA 70112, USA.
Shigeki SaitoTulane University Health Sciences Center, Department of Medicine, New Orleans, LA 70112, USA.
Bin ShanWashington State University-Spokane, Elson S. Floyd College of Medicine, Department of Biomedical Sciences, Spokane, WA 99210, USA.
Joseph A LaskyTulane University Health Sciences Center, Department of Medicine, New Orleans, LA 70112, USA. Electronic address: jlasky@tulane.edu.
Tulane University · USNational Institutes of Health · USWashington State University Spokane · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI JUDD E SHELLITO · 2012 to 2026
$69.1M
NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

Histone deacetylase 6 (HDAC6) regulates cytoplasmic signaling networks through deacetylation of various cytoplasmic substrates and serves as a key member of the ubiquitin proteasome system (UPS). This study is focused on HDAC6 regulation of the Notch1 receptor that plays a crucial role in tumor growth in NSCLC. A series of cell culture experiments were employed using A549, Lewis lung carcinoma 2 (LL2), and H1299 NSCLC cell lines to investigate HDAC6-mediated regulation of the Notch1 receptor through the UPS. HDAC6 was inhibited with small molecule inhibitors tubacin and ACY1215 in vitro and in vivo. Inhibition of HDAC6 led to reduced levels of Notch1 receptor in a dose-dependent manner in all three NSCLC cell lines tested. HDAC6 inhibition with ACY1215 led to G2 arrest, increased apoptosis, and increased levels of cleaved PARP1 in A549, LL2, and H1299 cell lines. In vivo inhibition of HDAC6 with ACY1215 significantly reduced LL2 tumor growth rate. Our data show that HDAC6 in NSCLC cells supports Notch1 signaling and promotes cell survival and proliferation. Our results support clinical investigation of HDAC6 inhibitors as a potential therapeutic option for treatment of NSCLC patients.

Identifiers

PMID31865176
PMCPMC6926313
OpenAlexW2996523818

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.