Evidence map›Paper›PMID 32102534›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2020

Apoptosis Induced by Prednisolone Occurs without Altering the Promoter Methylation of BAX and BCL-2 Genes in Acute Lymphoblastic Leukemia Cells CCRF-CEM.

Saiedeh Ganbarjeddi, Ako Azimi, Milad Zadi Heydarabad, Maryam Hemmatzadeh, Shahin Mohammadi, Reza Mousavi Ardehaie, Majid Zamani, Sina Baharaghdam, Sajjad Esmaeili, Amin Ghasemi

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Regulation of Apelin-13 on Bcl-2 and Caspase-3 and Its Effects on Adipocyte Apoptosis.Evidence-based complementary and alternative medicine : eCAM · 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

10 authors at 2 institutions in 1 country.

Saiedeh GanbarjeddiSchool of Medicine, Karazin Kharkiv National University, Kharkiv, Ukraine.
Ako AzimiDepartment of Basic Sciences, Maragheh University of Medical Sciences, Maragheh, Iran.ORCID 0000-0003-0962-818X
Milad Zadi HeydarabadMedicinal Plants Research Center, Yasuj University of Medical sciences, Yasuj, Iran.
Maryam HemmatzadehDepartment of Basic Sciences, Maragheh University of Medical Sciences, Maragheh, Iran.
Shahin MohammadiDepartment of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Reza Mousavi ArdehaieMedicinal Plants Research Center, Yasuj University of Medical sciences, Yasuj, Iran.
Majid ZamaniStudent Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Sina BaharaghdamImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sajjad EsmaeiliImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Amin GhasemiStudent Research Committee, Maragheh University of Medical Sciences, Maragheh, Iran.ORCID 0000-0001-9460-9615
Tabriz University of Medical Sciences · IRUniversity of Maragheh · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveone of the main mechanisms in which cancer cells are resistant to chemotherapy drugs and therapeutic strategies is resistance to apoptosis due to these anticancer factors. Regulating the expression of genes through epigenetics, especially regulation through methylation, is one of the key aspects of regulating gene expression and the function of genes, which is also regulated by the pathways regulating the pathway of apoptosis. The epigenetic regulatory phenomenon in cancer cells can undergo a change in regulation and induces resistance to apoptosis against chemotherapy and anticancer factors. The purpose of the present scrutiny was defined to probe the effect of subtoxic prednisolone dose on the level of promoter methylation and gene expression of BAX and BCL2 in the CCRF-CEM cells.

methodsThe treated cells by prednisolone, cultured in RPMI 1640 medium in standard condition. Alteration in promoter DNA methylation was analyzed by use of methylation specific-PCR (MSP) technique after the defined intervened time of Prednisolone treatment with a subtoxic dose.

resultsPrednisolone can induce apoptosis via alteration in BAX and BCL2 genes, based on our previous scrutiny. This essay shows no varies in the Pattern of DNA methylation of examined genes; however, prednisolone changes the expression of examined genes.

conclusionLack of alteration through prednisolone treatment in DNA methylation template of BAX and BCL2 genes make this possible that Prednisolone affects apoptotic gene expression via different pathways, which need more research to be done about it.<br />.

Indexed as

Antineoplastic Agents, HormonalApoptosisbcl-2-Associated X ProteinCell Line, TumorDNA MethylationDrug Resistance, NeoplasmGene ExpressionGene Expression Regulation, NeoplasticHumansPrecursor Cell Lymphoblastic Leukemia-LymphomaPrednisolonePromoter Regions, GeneticProto-Oncogene Proteins c-bcl-2Antineoplastic Agents, HormonalBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanPrednisoloneProto-Oncogene Proteins c-bcl-2Acute Lymphoblastic LeukemiaApoptosisDNA MethylationMethylation Specific PCR (MSP)Prednisolone

Identifiers

PMID32102534
PMCPMC7332151
OpenAlexW3006721522

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.