Evidence map›Paper›PMID 39630372›Full record

ArticleBiochemical genetics2025

AKR1B1 is Required for Maintaining Acute Leukemia Cell Survival by Epigenetic Silencing of Tumor Suppressor Genes.

Jingyu Chen, Lu Xu, Wangshi Li, Meiling Sun, Yao Chen, Ting Qiu, Yue Wu, Xingzhi Lv, Fukai Liu, Huitao Fan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Jingyu Chen *Department of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Lu Xu *Department of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Wangshi LiDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Meiling SunDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Yao ChenDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Ting QiuDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Yue WuDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Xingzhi LvDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Fukai LiuAnimal Laboratory Center, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Huitao FanDepartment of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China. huitaofan@hrbmu.edu.cn.

Funding

National Natural Science Foundation of China 82170164The First Affiliated Hospital of Harbin Medical University RC-GCC2021-001The National Key Research and Development Program of China 2022YFA1103300
6 · The paper itself

Abstract

AKR1B1 is a member of aldo-keto-reductase (AKR) superfamily which catalyze the reduction of carbonyl groups to hydroxyl groups in NADPH-dependent ways. Previous studies have shown that AKR1B1 promotes cancer progression, but its exact role in acute leukemia was unclear. Cell counting and Luminescent Cell Viability Assay were performed to measure the cell proliferation and viability. Soft-Agar Colony Formation (CFU) assay was conducted to measure the capacity of single cells to form colonies in vitro. Cell apoptosis, cell cycle, and cell differentiation were assessed by flow cytometry. Western blotting and RT-qPCR were utilized to examine AKR1B1 expression in acute leukemia cells. In vivo leukemia growth and mouse survival were evaluated using a model of xenotransplantation mice. We explored the AKR1B1 effect and mechanism in acute leukemia cells using RNA-sequencing technology and transcriptomic analysis. AKR1B1 is highly expressed in acute leukemia cells. Knockdown of AKR1B1 inhibited acute leukemia cell proliferation, colony-forming capability, and cell cycle and promoted apoptosis. Additionally, xenograft experiments proved that knockdown of AKR1B1 delayed the progression of acute leukemia cell in vivo. RNA-sequencing data analysis demonstrated that AKR1B1 was involved in the epigenetic silencing of H3K27me3-targeted genes. EZH2 inhibitor UNC1999 combined with knockdown of AKR1B1 showed synergistic inhibitory effect on acute leukemia cells. AKR1B1 is essential for the leukemogenesis and may serve as a potential therapeutic target to treat acute leukemia patients.

Indexed as

Epigenesis, GeneticGene SilencingGenes, Tumor SuppressorLeukemia, Myeloid, AcuteAldehyde ReductaseAldo-Keto ReductasesAnimalsApoptosisCell Line, TumorCell ProliferationCell SurvivalHumansMiceAKR1B1 protein, humanAldehyde ReductaseAldo-Keto ReductasesAcute LeukemiaAKR1B1EZH2H3K27me3UNC1999

Identifiers

PMID39630372
PMCPMC12602670

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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.