Evidence map›Paper›PMID 32788915›Full record

ArticleEXCLI journal2020

Effect of sodium butyrate on HDAC8 mRNA expression in colorectal cancer cell lines and molecular docking study of LHX1 - sodium butyrate interaction.

Flora Forouzesh, Mahsa Ghiaghi, Hamzeh Rahimi

Open access · greenAbstract read
In one paragraph

Article in EXCLI journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Sodium butyrate induces apoptosis enhanced by JAK2 inhibitor Fedratinib in NK/T-cell lymphoma cell.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Review
  3. Article
  4. LHX3 promotes EMT in hepatoma cell through β-catenin/TCF4 pathway.Medical oncology (Northwood, London, England) · 2024
    Article
  5. Article
  6. Review
  7. HDAC8 Promotes Liver Metastasis of Colorectal CancerOxidative medicine and cellular longevity · 2022
    Article
  8. 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

3 authors at 2 institutions in 1 country.

Flora ForouzeshDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Mahsa GhiaghiDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Hamzeh RahimiDepartment of Molecular Medicine, Pasteur Institute of Iran, Tehran, Iran.
Islamic Azad University Medical Branch of Tehran · IRPasteur Institute of Iran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most common type of cancer and the fourth leading cause of cancer related deaths worldwide. The Histone Deacetylase 8 (HDAC8) gene is a gene with unique features which can be used as a potential target for drug design. The LHX1 transcription factor is an important transcription factor for this gene. The aim of this study was to investigate the effect of sodium butyrate (NaB) as a histone deacetylase inhibitor (HDACi) on the expression of the HDAC8 gene in the colorectal cancer cell line, and the molecular docking of the LHX1 transcription factor with NaB. For this purpose, HCT-116 and HT-29 cell lines were treated with different concentrations of NaB (6.25 mM to 150 mM) at 24, 48 and 72 hours. Subsequently, RNA was extracted from the treated and untreated cells and cDNA was synthesized. Quantitative Real-Time-PCR was done to investigate the mRNA expression of HDAC8. Molecular docking was also performed to investigate the interaction between NaB and LHX1. Based on Real-time-PCR results, the concentration of 150 mM of NaB after 24 hours in HT-29 and HCT-116 cell lines caused a significant reduction in mRNA expression of HDAC8 (P<0.05). After 48 hours of treatment, there was a significant decrease in the mRNA expression of HDAC8 at all concentrations (P<0.05). The docking results showed that LHX1 and NaB interacted best at the lowest energy levels. Our results also showed that NaB bonded strongly to LHX1. In addition, our results demonstrated that NaB bound to the LHX1 transcription factor and inhibited the function of this factor and consequently decreased the transcription from the HDAC8 gene which resulted in cell death. Future studies are needed to assess the likely molecular mechanisms of NaB action on gene expression.

Indexed as

colorectal cancerdockingHCT-116 cell linesHDAC8 geneHT-29LHX1 transcription factorsodium butyrate

Identifiers

PMID32788915
PMCPMC7415931
OpenAlexW3072250448

What OpenQuestion holds

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LicenceCC BY
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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.