Evidence map›Paper›PMID 30982490›Full record

ArticleOncology research2019

MicroRNA-204 Potentiates the Sensitivity of Acute Myeloid Leukemia Cells to Arsenic Trioxide.

Zhiguo Wang, Zehui Fang, Runzhang Lu, Hongli Zhao, Tiejun Gong, Dong Liu, Luojia Hong, Jun Ma, Mei Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oncology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  3. Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025
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  4. Review
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  7. Review
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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 3 institutions in 1 country.

Zhiguo WangDepartment of Hematology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shanxi Province, P.R. China.
Zehui FangDepartment of Endocrinology, the 4th Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, P.R. China.
Runzhang LuDepartment of Bone Marrow Transplantation, Harbin Hematological Cancer Institute, Harbin the First Hospital, Harbin Province, P.R. China.
Hongli ZhaoDepartment of Endocrinology, the 4th Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, P.R. China.
Tiejun GongDepartment of Bone Marrow Transplantation, Harbin Hematological Cancer Institute, Harbin the First Hospital, Harbin Province, P.R. China.
Dong LiuDepartment of Bone Marrow Transplantation, Harbin Hematological Cancer Institute, Harbin the First Hospital, Harbin Province, P.R. China.
Luojia HongDepartment of Endocrinology, the 4th Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, P.R. China.
Jun MaDepartment of Bone Marrow Transplantation, Harbin Hematological Cancer Institute, Harbin the First Hospital, Harbin Province, P.R. China.
Mei ZhangDepartment of Hematology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shanxi Province, P.R. China.
Harbin Medical University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although arsenic trioxide (ATO) is a well-known antileukemic drug used for acute promyelocytic leukemia treatment, the development of ATO resistance is still a big challenge. We previously reported that microRNA-204 (miR-204) was involved in the regulation of acute myeloid leukemia (AML) cell apoptosis, but its role in chemoresistance is poorly understood. In the present study, we showed that miR-204 was significantly increased in AML cells after ATO treatment. Interestingly, the increased miR-204 level that was negatively correlated with ATO induced the decrease in cell viability and baculoviral inhibition of apoptosis protein repeat-containing 6 (BIRC6) expression. Overexpression of miR-204 potentiated ATO-induced AML cell growth inhibition and apoptosis. Furthermore, miR-204 directly targets to the 3'-UTR of BIRC6. Upregulation of miR-204 decreased BIRC6 luciferase activity and expression, which subsequently enhanced the expression of p53. Restoration of BIRC6 markedly reversed the effect of miR-204 on the regulation of AML cell sensitivity to ATO. Taken together, our study demonstrates that miR-204 decreases ATO chemoresistance in AML cells at least partially via promoting BIRC6/p53-mediated apoptosis. miR-204 represents a novel target of ATO, and upregulation of miR-204 may be a useful strategy to improve the efficacy of ATO in AML treatment.

Indexed as

Antineoplastic AgentsApoptosisArsenic TrioxideCell Line, TumorHL-60 CellsHumansInhibitor of Apoptosis ProteinsLeukemia, Myeloid, AcuteMicroRNAsTumor Suppressor Protein p53Up-RegulationAntineoplastic AgentsArsenic TrioxideBIRC6 protein, humanInhibitor of Apoptosis ProteinsMicroRNAsMIRN204 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30982490
PMCPMC7848422
OpenAlexW2939901635

What OpenQuestion holds

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Registered trials

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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.