Evidence map›Paper›PMID 25781604›Full record

ArticlePloS one2015

Epigenetic modulation with HDAC inhibitor CG200745 induces anti-proliferation in non-small cell lung cancer cells.

Sung-Min Chun, Ji-Young Lee, Jene Choi, Je-Hwan Lee, Jung Jin Hwang, Chung-Soo Kim, Young-Ah Suh, Se Jin Jang

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Histone Deacetylase Inhibition in Non-small Cell Lung Cancer: Hype or Hope?Frontiers in cell and developmental biology · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Histone deacetylase inhibitor, CG200745, attenuates cardiac hypertrophy and fibrosis in DOCA-induced hypertensive rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  20. 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

8 authors.

Sung-Min ChunDepartment of Pathology, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Ji-Young LeeAsan Institute for Life Science, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Jene ChoiDepartment of Pathology, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Je-Hwan LeeDepartment of Oncology, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Jung Jin HwangAsan Institute for Life Science, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Chung-Soo KimDepartment of Urology, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Young-Ah SuhAsan Institute for Life Science, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.
Se Jin JangDepartment of Pathology, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea; Asan Institute for Life Science, Asan Medical Center, The University of Ulsan College of Medicine, Seoul, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone modification plays a pivotal role on gene regulation, as regarded as global epigenetic markers, especially in tumor related genes. Hence, chemical approaches targeting histone-modifying enzymes have emerged onto the main stage of anticancer drug discovery. Here, we investigated the therapeutic potentials and mechanistic roles of the recently developed histone deacetylase inhibitor, CG200745, in non-small cell lung cancer cells. Treatment with CG200745 increased the global level of histone acetylation, resulting in the inhibition of cell proliferation. ChIP-on-chip analysis with an H4K16ac antibody showed altered H4K16 acetylation on genes critical for cell growth inhibition, although decreased at the transcription start site of a subset of genes. Altered H4K16ac was associated with changes in mRNA expression of the corresponding genes, which were further validated in quantitative RT-PCR and western blotting assays. Our results demonstrated that CG200745 causes NSCLC cell growth inhibition through epigenetic modification of critical genes in cancer cell survival, providing pivotal clues as a promising chemotherapeutics against lung cancer.

Indexed as

AcetylationApoptosisBlotting, WesternCarcinoma, Non-Small-Cell LungCell CycleCell DifferentiationCell ProliferationChromatin ImmunoprecipitationEpigenomicsGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistonesHumansHydroxamic AcidsLung NeoplasmsNaphthalenesHistone Deacetylase InhibitorsHistonesHydroxamic AcidsN1-(3-(dimethylamino)propyl)-N8-hydroxy-2-((naphthalene-1-loxy)methyl)oct-2-enediamideNaphthalenesRNA, Messenger

Identifiers

PMID25781604
PMCPMC4363698

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.