Evidence map›Paper›PMID 25946558›Full record

ArticleMolecules (Basel, Switzerland)2015

NBM-T-BBX-OS01, Semisynthesized from Osthole, Induced G1 Growth Arrest through HDAC6 Inhibition in Lung Cancer Cells.

Jih-Tung Pai, Chia-Yun Hsu, Kuo-Tai Hua, Sheng-Yung Yu, Chung-Yang Huang, Chia-Nan Chen, Chiung-Ho Liao, Meng-Shih Weng

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2015. 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
0.6field-weighted citation impact, top 31% 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, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Histone deacetylase inhibitor MPT0B291 suppresses Glioma GrowthInternational journal of biological sciences · 2020
    Article
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  10. Article
  11. Review
  12. 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.

Jih-Tung PaiDivision of Hematology and Oncology, Tao-Yuan General Hospital, Ministry of Health and Welfare, Taoyuan City 33004, Taiwan. jihtungpai@gmail.com.
Chia-Yun HsuDepartment of Nutritional Science, Fu Jen Catholic University, New Taipei City 24205, Taiwan. sandy0805w@hotmail.com.
Kuo-Tai HuaGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan. d94447003@gmail.com.
Sheng-Yung YuDepartment of Nutritional Science, Fu Jen Catholic University, New Taipei City 24205, Taiwan. j06103@hotmail.com.
Chung-Yang HuangNatureWise Biotech and Medicals Corporation, Taipei 11559, Taiwan. naturewisecyh@gmail.com.
Chia-Nan ChenNatureWise Biotech and Medicals Corporation, Taipei 11559, Taiwan. alex_chen@gnt.com.tw.
Chiung-Ho LiaoDivision of Drug and New Technology Product, Food and Drug Administration, Ministry of Health and Welfare, Executive Yuan, Taipei 11516, Taiwan. cedar@fda.gov.tw.
Meng-Shih WengDepartment of Nutritional Science, Fu Jen Catholic University, New Taipei City 24205, Taiwan. 078670@mail.fju.edu.tw.
Fu Jen Catholic University · TWMinistry of Health and Welfare · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disrupting lung tumor growth via histone deacetylases (HDACs) inhibition is a strategy for cancer therapy or prevention. Targeting HDAC6 may disturb the maturation of heat shock protein 90 (Hsp90) mediated cell cycle regulation. In this study, we demonstrated the effects of semisynthesized NBM-T-BBX-OS01 (TBBX) from osthole on HDAC6-mediated growth arrest in lung cancer cells. The results exhibited that the anti-proliferative activity of TBBX in numerous lung cancer cells was more potent than suberoylanilide hydroxamic acid (SAHA), a clinically approved pan-HDAC inhibitor, and the growth inhibitory effect has been mediated through G1 growth arrest. Furthermore, the protein levels of cyclin D1, CDK2 and CDK4 were reduced while cyclin E and CDK inhibitor, p21Waf1/Cip1, were up-regulated in TBBX-treated H1299 cells. The results also displayed that TBBX inhibited HDAC6 activity via down-regulation HDAC6 protein expression. TBBX induced Hsp90 hyper-acetylation and led to the disruption of cyclin D1/Hsp90 and CDK4/Hsp90 association following the degradation of cyclin D1 and CDK4 proteins through proteasome. Ectopic expression of HDAC6 rescued TBBX-induced G1 arrest in H1299 cells. Conclusively, the data suggested that TBBX induced G1 growth arrest may mediate HDAC6-caused Hsp90 hyper-acetylation and consequently increased the degradation of cyclin D1 and CDK4.

Indexed as

AcetylationCell Cycle CheckpointsCell Line, TumorCell ProliferationCoumarinsCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21Down-RegulationG1 PhaseHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesHSP90 Heat-Shock ProteinsHumansHydroxamic AcidsCDK2 protein, humanCDK4 protein, humanCoumarinsCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21HDAC6 protein, humanHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesHSP90 Heat-Shock ProteinsHydroxamic AcidsostholProteasome Endopeptidase Complex

Identifiers

PMID25946558
PMCPMC6272357
OpenAlexW2101721092

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.