Evidence map›Paper›PMID 34319031›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2021

Effect of Decitabine (5-aza-2'-deoxycytidine, 5-aza-CdR) in Comparison with Vorinostat (Suberoylanilide Hydroxamic Acid, SAHA) on DNMT1, DNMT3a and DNMT3b, HDAC 1-3, SOCS 1, SOCS 3, JAK2, and STAT3 Gene Expression in Hepatocellular Carcinoma HLE and LCL-PI 11 Cell Lines.

Masumeh Sanaei, Fraidoon Kavoosi, Mohammad Pourahmadi

Open access · goldAbstract readComparative Study
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2021. 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
0.8field-weighted citation impact, top 29% 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, 14 citations in OpenAlex.

  1. FANCD2 promotes wound healing through DNMT1.Histochemistry and cell biology · 2026
    Article
  2. Review
  3. Review
  4. Targeting one-carbon metabolism for cancer immunotherapy.Clinical and translational medicine · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. The Relevance ofDiagnostics (Basel, Switzerland) · 2021
    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.

Masumeh SanaeiResearch Center for Non-Communicable Diseases, Jahrom University of Medical Sciences, Jahrom, Iran.
Fraidoon KavoosiResearch Center for Non-Communicable Diseases, Jahrom University of Medical Sciences, Jahrom, Iran.
Mohammad PourahmadiDepartments of Anatomical Sciences, Jahrom University of Medical Sciences, Jahrom, Iran.
Jahrom University of Medical Sciences · IRJahrom University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpigenetic alterations play an important role in tumorigenesis. Hypermethylation of CpG islands within the promoter regions of tumor suppressor genes (TSGs) and histone deacetylation lead to the silencing of the genes resulting in cancer induction. The suppressor of cytokine signaling (SOCS) family is an important negative regulator of cytokine signaling and deregulation of this family has been reported in several cancers, the protein of the SOCS family inhibit the cytokine-activated Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway to modulate cellular responses. Previously, we evaluated the effects of DNA demethylating agents and histone deacetylase inhibitors on hepatocellular carcinoma (HCC). The current study aimed to investigate the effect of decitabine (5-aza-2'-deoxycytidine, 5-aza-CdR) in comparison to vorinostat (suberoylanilide hydroxamic acid, SAHA) on DNMT1, DNMT3a and DNMT3b, HDAC 1-3, SOCS 1, SOCS 3, JAK2, and STAT3 gene expression, cell growth inhibition, and apoptosis induction of HCC HLE and LCL-PI 11 cell lines. MATERIAL AND

methodsThe HLE and LCL-PI 11 cells were treated with 5-aza-CdR and SAHA and then the MTT assay, flow cytometry assay, and quantitative real-time RT-PCR were achieved to determine cell viability, cell apoptosis, and relative gene expression respectively.

resultsThe result indicated that both compounds inhibited cell growth, induced apoptosis, and down-regulated DNMT1, DNMT3a DNMT3b, HDAC 1-3, JAK2, and STAT3 and up-regulated HDAC 1-3, SOCS 1, and SOCS 3 genes expression significantly. The apoptotic effect of SAHA was stronger than that of 5-Aza-CdR.

conclusion5-Aza-CdR and SAHA can induce cell growth inhibition and apoptosis induction through the JAK/STAT pathway.

Indexed as

Antigens, NeoplasmApoptosisCarcinoma, HepatocellularCarrier ProteinsCell Line, TumorCell SurvivalDecitabineGene ExpressionHistone DeacetylasesHumansJanus KinasesLiver NeoplasmsRepressor ProteinsSignal TransductionSTAT Transcription FactorsVorinostatAntigens, NeoplasmCarrier ProteinsDecitabineHistone DeacetylasesJanus KinasesRepressor ProteinsSTAT Transcription FactorsUBXN11 protein, humanVorinostatDecitabineHCCJAK/STATSOCSvorinostat

Identifiers

PMID34319031
PMCPMC8607106
OpenAlexW3184567356

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.