Evidence map›Paper›PMID 22072212›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012

Alteration in miRNA gene expression pattern in acute promyelocytic leukemia cell induced by arsenic trioxide: a possible mechanism to explain arsenic multi-target action.

Seyed H Ghaffari, Davood Bashash, Majid Zaki Dizaji, Ardeshir Ghavamzadeh, Kamran Alimoghaddam

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  7. Exposure to arsenite and cadmium induces organotoxicity and miRNAs deregulation in male rats.Environmental science and pollution research international · 2020
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  20. Analysis of the transcriptome in molecular epidemiology studies.Environmental and molecular mutagenesis · 2013
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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

5 authors at 2 institutions in 1 country.

Seyed H GhaffariHematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran. shghaffari200@yahoo.com
Davood Bashash
Majid Zaki Dizaji
Ardeshir Ghavamzadeh
Kamran Alimoghaddam
Tehran University of Medical Sciences · IRShariati Hospital · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are involved in cancer pathogenesis, apoptosis, and cell growth, and these miRNAs are thought to be functional as oncogenes and/or tumor suppressors in the gene regulatory networks. We studied the potential contribution of miRNAs in acute promyelocytic leukemia (APL) cell NB4 during the apoptosis induction by arsenic trioxide (ATO). The apoptotic effects of ATO on the NB4 cell line at a pharmacological dose (2 μM) was verified using cell growth and viability assays, MTT assay, BrdU cell proliferation assay, flow cytometric analysis, and caspase-3 activity assay. miRNAs from untreated and 2 μM ATO-treated NB4 cell line were extracted, purified, and converted to complementary DNAs. Differential expressions of 88 cancer-related miRNAs were analyzed by real-time reverse transcription PCR using miRNA PCR cancer-array system. After normalizing to the average Ct value of three housekeeping genes in the array (U6, SNORD47, and SNORD48), the fold change of miRNAs was calculated in the ATO-treated cells as compared to untreated. Among the 88 cancer-focused miRNAs, 51 miRNAs were found to be differentially expressed more than 2-fold after ATO treatment. Of these, 48 miRNAs were upregulated up to 21.65-fold changes, while three miRNAs were downregulated up to 5.19-fold changes. By screening the literature, a majority of these upregulated miRNAs were found to have tumor and/or metastatic suppressors' functions associated with cell cycle arrest and apoptosis, as well as inhibition of angiogenesis, invasion, and metastasis. Our results demonstrate that ATO, at the relevant concentration, modulate a substantial number of cancer-related miRNAs in APL cell line; most of these are known to function as a tumor and/or metastatic suppressors and have confirmed targets involved in cell cycle arrest and apoptosis. The results of this study support the hypothesis that miRNAs may play a mediatory role in eliciting the multi-target and pleiotropic action of ATO.

Indexed as

Antineoplastic AgentsApoptosisArsenicalsArsenic TrioxideCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene ExpressionHumansLeukemia, Promyelocytic, AcuteMicroRNAsOxidesAntineoplastic AgentsArsenicalsArsenic TrioxideMicroRNAsOxides

Identifiers

PMID22072212
OpenAlexW2057269218

What OpenQuestion holds

Textmetadata
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.