Evidence map›Paper›PMID 31572009›Full record

ArticleCancer management and research2019

ADAR1 may be involved in the proliferation of acute myeloid leukemia cells via regulation of the Wnt pathway.

Han Xiao, Qian Cheng, Xinyu Wu, Yishu Tang, Jing Liu, Xin Li

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 33% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  9. Review
  10. RNA binding proteins in MLL-rearranged leukemia.Experimental hematology & oncology · 2022
    Review
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  14. Review
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

6 authors at 2 institutions in 1 country.

Han XiaoDepartment of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Qian ChengDepartment of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Xinyu WuDepartment of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Yishu TangDepartment of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Jing LiuDepartment of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Xin LiDepartment of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Central South University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAcute myeloid leukemia (AML) is the most common type of leukemia and characterized by the malignant growth of leukemic cells. Adenosine deaminases acting on RNA 1 (ADAR1) have been shown to participate in the proliferation of cancer cells and progression of various cancers. However, the role of ADAR1 in AML has not been investigated. PATIENTS AND

methodsWe compared the expression levels of ADAR1 between samples obtained from different AML patients and controls using quantitative-polymerase chain reaction and Western blotting. We also investigated the functional role and possible mechanisms via silencing the expression of ADAR1 in vitro and in vivo.

resultsWe found that the mRNA and protein levels of ADAR1 were significantly higher in AML patients. The mRNA expression of ADAR1 was positively correlated with the ratio of leukemic cells. Additionally, silencing of ADAR1 expression significantly suppressed the proliferation of AML cells and induced G0/1 arrest. For the analysis of the mechanism, the quantitative-polymerase chain reaction and Western blotting results revealed that ADAR1 knockdown resulted in the decreased expression of Wingless-Int (Wnt) effectors including β-catenin, c-Myc, transcription factor 4, and cyclin D2. In the nude mouse model, inhibition of ADAR1 expression reduced the tumorigenic potential and decreased the expression o]f Wnt effectors.

conclusionThese results demonstrate that ADAR1 may be involved in the regulation of the proliferation of AML cells partially via regulation of the Wnt signaling pathway.

Indexed as

acute myeloid leukemiaADAR1cell cycleproliferationWnt pathway

Identifiers

PMID31572009
PMCPMC6759212
OpenAlexW2974374361

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.