Evidence map›Paper›PMID 28099148›Full record

ArticleOncotarget2017

Suberoylanilide hydroxamic acid increases anti-cancer effect of tumor necrosis factor-α through up-regulation of TNF receptor 1 in lung cancer cells.

Bo Ra You, Bo Ram Han, Woo Hyun Park

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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  7. [Alkaline processing of cantharidin can significanty improve the antitumor activity of cantharidin].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
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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

3 authors at 1 institution in 1 country.

Bo Ra YouDepartment of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, Jeonju, 561-180, Republic of Korea.
Bo Ram HanDepartment of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, Jeonju, 561-180, Republic of Korea.
Woo Hyun ParkDepartment of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, Jeonju, 561-180, Republic of Korea.
Jeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Suberoylanilide hydroxamic acid (SAHA) as a histone deacetylase (HDAC) inhibitor has anti-cancer effect. Here, we evaluated the effect of SAHA on HDAC activity and cell growth in many normal lung and cancer cells. We observed that the HDAC activities of lung cancer cells were higher than that of normal lung cells. SAHA inhibited the growth of lung cancer cells regardless of the inhibitory effect on HDAC. This agent induced a G2/M phase arrest and apoptosis, which was accompanied by mitochondrial membrane potential (MMP: ΔΨm) loss in lung cancer cells. However, SAHA did not induce cell death in normal lung cells. All tested caspase inhibitors prevented apoptotic cell death in SAHA-treated A549 and Calu-6 lung cancer cells. Treatment with tumor necrosis factor-alpha (TNF-α) enhanced apoptosis in SAHA-treated lung cancer cells through caspase-8 and caspase-9 activations. Especially, SAHA increased the expression level of TNF-α receptor 1 (TNFR1), especially acetylation of the region of TNFR1 promoter -223/-29 in lung cancer cells. The down-regulation of TNFR1 suppressed apoptosis in TNF-α and SAHA-treated lung cancer cells. In conclusion, SAHA inhibited the growth of lung cancer cells via a G2/M phase arrest and caspase-dependent apoptosis. SAHA also enhanced apoptotic effect of TNF-α in human lung cancer cells through up-regulation of TNFR1. TNF-α may be a key to improve anti-cancer effect of HDAC inhibitors.

Indexed as

A549 CellsAcetylationAntineoplastic AgentsApoptosisCaspase 8Caspase 9Cell Line, TumorCell ProliferationEnzyme ActivationG2 Phase Cell Cycle CheckpointsHistone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsLung NeoplasmsMembrane Potential, MitochondrialAntineoplastic AgentsCaspase 8Caspase 9Histone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsReceptors, Tumor Necrosis Factor, Type ITumor Necrosis Factor-alphaVorinostatapoptosishistone deacetylaselung cancersuberoylanilide hydroxamic acidtumor necrosis factor-α

Identifiers

PMID28099148
PMCPMC5392281
OpenAlexW2572843927

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.