Evidence map›Paper›PMID 37316630›Full record

ArticleActa pharmacologica Sinica2023

Chloroquine enhances the efficacy of chemotherapy drugs against acute myeloid leukemia by inactivating the autophagy pathway.

Han-Lin Wang, Jia-Nan Li, Wei-Juan Kan, Gao-Ya Xu, Guang-Hao Luo, Ning Song, Wen-Biao Wu, Bo Feng, Jing-Feng Fu, Yu-Tong Tu and 5 more

Open access · greenAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 23 citations in OpenAlex.

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  16. Advancements in programmed cell death research in antitumor therapy: a comprehensive overview.Apoptosis : an international journal on programmed cell death · 2025
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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

15 authors at 5 institutions in 2 countries.

Han-Lin WangSchool of Pharmacy, Fudan University, Shanghai, 210023, China.
Jia-Nan LiSchool of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Wei-Juan KanState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Gao-Ya XuSchool of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Guang-Hao LuoState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Ning SongState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Wen-Biao WuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Bo FengState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Jing-Feng FuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Yu-Tong TuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Min-Min LiuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Ran XuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Yu-Bo ZhouState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. ybzhou@simm.ac.cn.
Gang WeiSchool of Pharmacy, Fudan University, Shanghai, 210023, China. weigang@shmu.edu.cn.
Jia LiSchool of Pharmacy, Fudan University, Shanghai, 210023, China. jli@simm.ac.cn.
Chinese Academy of Sciences · CNNanjing University of Chinese Medicine · CNShanghai Institute of Materia Medica · CNUniversity of Chinese Academy of Sciences · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current therapy for acute myeloid leukemia (AML) is largely hindered by the development of drug resistance of commonly used chemotherapy drugs, including cytarabine, daunorubicin, and idarubicin. In this study, we investigated the molecular mechanisms underlying the chemotherapy drug resistance and potential strategy to improve the efficacy of these drugs against AML. By analyzing data from ex vivo drug-response and multi-omics profiling public data for AML, we identified autophagy activation as a potential target in chemotherapy-resistant patients. In THP-1 and MV-4-11 cell lines, knockdown of autophagy-regulated genes ATG5 or MAP1LC3B significantly enhanced AML cell sensitivity to the chemotherapy drugs cytarabine, daunorubicin, and idarubicin. In silico screening, we found that chloroquine phosphate mimicked autophagy inactivation. We showed that chloroquine phosphate dose-dependently down-regulated the autophagy pathway in MV-4-11 cells. Furthermore, chloroquine phosphate exerted a synergistic antitumor effect with the chemotherapy drugs in vitro and in vivo. These results highlight autophagy activation as a drug resistance mechanism and the combination therapy of chloroquine phosphate and chemotherapy drugs can enhance anti-AML efficacy.

Indexed as

IdarubicinLeukemia, Myeloid, AcuteAntineoplastic Combined Chemotherapy ProtocolsAutophagyChloroquineCytarabineDaunorubicinHumansChloroquineCytarabineDaunorubicinIdarubicinacute myeloid leukemiaautophagychloroquine phosphatecytarabinedaunorubicindrug resistantidarubicinmulti-omics

Identifiers

PMID37316630
PMCPMC10618541
OpenAlexW4380609146

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.