Evidence map›Paper›PMID 36144542›Full record

ArticleMolecules (Basel, Switzerland)2022

The Identification of APOBEC3G as a Potential Prognostic Biomarker in Acute Myeloid Leukemia and a Possible Drug Target for Crotonoside.

Chenchen Ma, Peng Liu, Siyuan Cui, Chang Gao, Xing Tan, Zhaopeng Liu, Ruirong Xu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-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

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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. 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

7 authors at 4 institutions in 1 country.

Chenchen MaCentral Laboratory of Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China.ORCID 0000-0001-7631-4880
Peng LiuDepartment of Laboratory Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan 250014, China.
Siyuan CuiDepartment of Hematology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China.
Chang GaoFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan 250014, China.
Xing TanFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan 250014, China.
Zhaopeng LiuDepartment of Medicinal Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University, Jinan 250014, China.ORCID 0000-0001-9429-8028
Ruirong XuDepartment of Hematology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China.ORCID 0000-0002-9871-1542
Shandong University of Traditional Chinese Medicine · CNAffiliated Hospital of Shandong University of Traditional Chinese Medicine · CNShandong Provincial QianFoShan Hospital · CNShandong University · CN

Funding

National Natural Science Foundation of China 81903984National Natural Science Foundation of China 8197141791Natural Science Foundation of Shandong Province ZR2019PH018
6 · The paper itself

Abstract

The apolipoprotein B mRNA editing enzyme catalytic subunit 3G (APOBEC3G) converts cytosine to uracil in DNA/RNA. Its role in resisting viral invasion has been well documented. However, its expression pattern and potential function in AML remain unclear. In this study, we carried out a bioinformatics analysis and revealed that the expression of APOBEC3G was significantly upregulated in AML, and high expression of APOBEC3G was significantly associated with short overall survival (OS). APOBEC3G expression was especially increased in non-M3AML, and correlated with the unfavorable cytogenetic risks. Additionally, Cox regression analyses indicated APOBEC3G is a hazard factor that cannot be ignored for OS of AML patients. In molecular docking simulations, the natural product crotonoside was found to interact well with APOBEC3G. The expression of APOBEC3G is the highest in KG-1 cells, and the treatment with crotonoside can reduce the expression of APOBEC3G. Crotonoside can inhibit the viability of different AML cells in vitro, arrest KG-1 and MV-4-11 cells in the S phase of the cell cycle and affect the expression of cycle-related proteins, and induce cell apoptosis. Therefore, APOBEC3G could be a potential drug target of crotonoside, and crotonoside can be considered as a lead compound for APOBEC3G inhibition in non-M3 AML.

Indexed as

Biological ProductsHIV-1Leukemia, Myeloid, AcuteAdenosineAPOBEC-1 DeaminaseAPOBEC-3G DeaminaseBiomarkersCytidine DeaminaseCytosineGuanosineHumansMolecular Docking SimulationPrognosisRNAUracilAdenosineAPOBEC-1 DeaminaseAPOBEC-3G DeaminaseAPOBEC3G protein, humanBiological ProductsBiomarkersCytidine DeaminaseCytosineGuanosineisoguanosineRNAUracilAMLanti-tumor activitiesapolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) genebioinformatics analysiscrotonosideprognosis

Identifiers

PMID36144542
PMCPMC9503540
OpenAlexW4295007353

What Socratic 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 Socratic graph.