Evidence map›Paper›PMID 41896383›Full record

ArticleScientific reports2026

The fluoroquinoline compound exerts anti-erythroleukemic effects by dual-targeting GLUT1 and the PI3K/AKT signaling pathway.

Sha Cheng, Weijia Zhao, Jia Yu, Xueling Meng, Bixue Xu, Ningning Zan, Baofei Sun, Heng Luo

Abstract read
In one paragraph

Article in Scientific reports, 2026. 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

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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

8 authors.

Sha Cheng *State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China.
Weijia Zhao *State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China.
Jia YuState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China.
Xueling MengState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China.
Bixue XuState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China.
Ningning ZanState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China. zan11658@163.com.
Baofei SunState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China. 1589894559@qq.com.
Heng LuoState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, 550014, Guizhou, China. luoheng71050@aliyun.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythroleukemia is a rare hematological malignancy in clinical practice, and currently, there are no effective treatment options other than stem cell transplantation. The study found that the fluoroquinoline compound FKL-137 can significantly inhibit the proliferation of erythroleukemia cells and induce apoptosis in vitro, while in vivo, it prevents the development of Friend virus-induced erythroleukemia and splenomegaly in mice. Mechanistic studies revealed that FKL-137 reduces glucose uptake and lactate secretion in erythroleukemia cells by targeting GLUT1 and inhibits the expression of glucose metabolism-related proteins, including PKM2, HK2, and LDH. Additionally, FKL-137 modulates the PI3K/AKT signaling pathway, which is closely associated with GLUT1. These results highlight the critical role of GLUT1 in the growth and survival of erythroleukemia and demonstrate that FKL-137 exerts its regulatory effects on glucose metabolism through the dual-targeting of GLUT1 and the PI3K/AKT signaling pathway, making it a potential therapeutic agent for erythroleukemia.

Indexed as

Antineoplastic AgentsGlucose Transporter Type 1Leukemia, Erythroblastic, AcutePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsApoptosisCell Line, TumorCell ProliferationGlucoseHumansMiceAntineoplastic AgentsGlucoseGlucose Transporter Type 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSLC2A1 protein, humanErythroleukemiaFluoroquinolineGlucose metabolismGLUT1GlycolysisPI3K/AKT

Identifiers

PMID41896383
PMCPMC13039185

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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.