Evidence map›Paper›PMID 38217769›Full record

ArticleMolecular biology reports2024

siRNA-mediated downregulation of BATF3 diminished proliferation and induced apoptosis through downregulating c-Myc expression in chronic myelogenous leukemia cells.

Reza Dabbaghipour, Vahid Khaze Shahgoli, Sahar Safaei, Mohammad Amini, Smb Tabei, Dariush Shanehbandi, Omid Rahbar Farzam, Behzad Baradaran, Mona Entezam

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

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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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. c-Medical sciences (Basel, Switzerland) · 2026
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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

9 authors at 2 institutions in 2 countries.

Reza DabbaghipourDepartment of Medical Genetics, Shiraz University of Medical Sciences, Shiraz, Iran.
Vahid Khaze ShahgoliImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sahar SafaeiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad AminiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Smb TabeiDepartment of Medical Genetics, Shiraz University of Medical Sciences, Shiraz, Iran.
Dariush ShanehbandiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Omid Rahbar FarzamImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Behzad BaradaranImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. baradaranb@tbzmed.ac.ir.ORCID http://orcid.org/0000-0002-8642-6795
Mona EntezamDepartment of Medical Genetics, Shiraz University of Medical Sciences, Shiraz, Iran. entezam@sums.ac.ir.
Tabriz University of Medical Sciences · IRShiraz University of Medical Sciences · IR

Funding

We didn't receive grant for this research. We didn't receive grant for this research.
6 · The paper itself

Abstract

objectiveDespite considerable improvement in therapeutic approaches to chronic myeloid leukemia (CML) treatment, this malignancy is considered incurable due to resistance. However, investigating the molecular mechanism of CML may give rise to the development of extremely efficient targeted therapies that improve the prognosis of patients. Basic leucine zipper transcription factor ATF-like3 (BATF3), as transcription factor, is considered a key regulator of cellular activities and its function has been evaluated in tumor development and growth in several cancer types. This study aimed to evaluate the potential of the cellular impact of siRNA-mediated downregulation of BATF3 on CML cancer cells through cell proliferation, induction of apoptosis, and cell cycle distribution. MATERIALS AND

methodsThe transfection of BATF3 siRNA to K562 CML cells was performed by electroporation device. To measure cellular viability and apoptosis, MTT assay and Annexin V/PI staining were carried out, respectively. Also, cell cycle assay and flow cytometry instrument were applied to assess cell cycle distribution of K562 cells. For more validation, mRNA expression of correlated genes was relatively evaluated by quantitative real-time polymerase chain reaction (qRT-PCR).

resultsThe data indicated that siRNA-mediated BATF3 inactivating severely promoted the cell apoptosis. Also, the targeted therapy led to high expression of Caspase-3 gene and Bax/Bcl-2 ratio. Silenced BATF3 also induced cell cycle arrest in phase sub-G1 compared to control. Finally, a noticeable decrement was obtained in c-Myc gene expression through suppression of BATF3 in CML cells.

conclusionThe findings of this research illustrated the suppression of BATF3 as an effective targeted therapy strategy for CML.

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveApoptosisBasic-Leucine Zipper Transcription FactorsCell ProliferationDown-RegulationHumansRepressor ProteinsRNA, Small InterferingBasic-Leucine Zipper Transcription FactorsBATF3 protein, humanRepressor ProteinsRNA, Small InterferingApoptosisBATF3Cell proliferationChronic myeloid leukemiac-Myc

Identifiers

PMID38217769
OpenAlexW4390841422

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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.