Evidence map›Paper›PMID 23867991›Full record

ArticleMolecular and cellular biochemistry2013

Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer.

Chi-Qi Chen, Cheng-Shui Chen, Jun-Jie Chen, Lian-Ping Zhou, Hong-Lei Xu, Wei-Wei Jin, Jian-Bo Wu, Shen-Meng Gao

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Deleted in lymphocytic leukemia 2 (DLEU2): a possible biomarker that holds promise for future diagnosis and treatment of cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  7. Review
  8. Research progress in effects of microRNAZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. Review
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  15. Review
  16. Low miR-16 expression induces regulatory CD4American journal of cancer research · 2021
    Article
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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

8 authors at 3 institutions in 1 country.

Chi-Qi ChenLaboratory of Internal Medicine, The First Affiliated Hospital of Wenzhou Medical College, 2, FuXue Road, Wenzhou, 325000, China.
Cheng-Shui Chen
Jun-Jie Chen
Lian-Ping Zhou
Hong-Lei Xu
Wei-Wei Jin
Jian-Bo Wu
Shen-Meng Gao
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNWenzhou Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylases (HDACs) inhibitor is a promising new approach to the treatment of lung cancer therapy via inhibiting cell growth and inducing apoptosis. miR-15a and miR-16-1 are important tumor suppressors through modulating B cell lymphoma 2 (Bcl-2), Cyclin D1, D2, and others. However, whether HDACs inhibitor modulates the expression of miR-15a/16-1 in lung cancer is still unknown. The purpose of our study was to identify a new miRNA-mediated mechanism which plays an important role in the anti-cancer effects of HDACs inhibitor. We found HDACs inhibitors trichostatin A (TSA) and sodium butyrate upregulated the expression of miR-15a/16-1, residing in the host tumor suppressor Dleu2 gene, through increasing the histone acetylation in the region of Dleu2/miR-15a/16-1 promoter in lung cancer cells. Moreover, among class Ι HDACs subtypes, only knockdown of HDAC3 by specific siRNA increased the hyperacetylation of Dleu2/miR-15a/16-1 promoter region and finally resulted in the upregulation of miR-15a/16-1. Furthermore, overexpression of miR-15a/16-1, which were always deleted or downregulated in lung cancer cells, effectively suppressed cell growth and reduced colony formation. Finally, TSA reduced the expression of Bcl-2, an important survival protein in lung cancer cells, partly through upregulation of miR-15a/16-1. Therefore, this offers a therapeutic strategy that lung cancer patients who exhibit low level of miR-15a/16-1 or high activity of HDACs may benefit from HDACs inhibitor-based therapy.

Indexed as

AcetylationApoptosisButyric AcidCarcinoma, Non-Small-Cell LungCell Cycle CheckpointsCell Line, TumorCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansHydroxamic AcidsButyric AcidDLEU2 lncRNA, humanHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsMicroRNAsMIRN15 microRNA, humanMIRN16 microRNA, humanProto-Oncogene Proteins c-bcl-2RNA, Long NoncodingTransferasestrichostatin ATumor Suppressor Proteins

Identifiers

PMID23867991
OpenAlexW2050843217

What OpenQuestion holds

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Registered trials

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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.