Evidence map›Paper›PMID 39384125›Full record

ArticleJournal of advanced research2025

Integrated stress response activation induced by usnic acid alleviates BCL-2 inhibitor ABT-199 resistance in acute myeloid leukemia.

Dijiong Wu, Man Li, Yaonan Hong, Li Jin, Qi Liu, Chengtao Sun, Liqin Li, Xiaoxiao Han, Shengqian Deng, Yue Feng and 2 more

Abstract read
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

12 authors.

Dijiong WuDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China; Zhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China. Electronic address: wudijiong@zcmu.edu.cn.
Man LiDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China; Zhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Yaonan HongDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Li JinZhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Qi LiuDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Chengtao SunZhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Liqin LiKey Laboratory of Traditional Chinese Medicine for the Development and Clinical Transformation of Immunomodulatory Traditional Chinese Medicine in Zhejiang Province, Huzhou Central Hospital, the Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, Zhejiang, China.
Xiaoxiao HanZhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Shengqian DengZhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Yue FengZhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Yiping ShenDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Guoyin KaiDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China; Zhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China. Electronic address: kaiguoyin@zcmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionABT-199 (venetoclax) is a BCL-2 suppressor with pronounced effects on acute myeloid leukemia (AML). However, its usefulness as a monotherapy or in combination with hypomethylating medicines like azacitidine is debatable due to acquired resistance. Usnic acid, a dibenzofuran extracted from lichen Usnea diffracta Vain, exhibits anticancer properties and may counteract multidrug resistance in leukemia cells.

objectiveThis study investigated whether usnic acid at low-cytotoxicity level could enhance sensitivity of AML cells with acquired resistance to ABT-199 by targeting the integrated stress response pathways.

methodsTo investigate the combined effects on AML cells, we used a cell viability test, flow cytometry to quantify apoptosis, cell cycle analysis, and mitochondrial membrane potential measurement. RNA-seq and immunoblot were used to determine the potential mechanisms of ABT-199 + usnic acid combination.

resultsUsnic acid, at a low cytotoxicity level, successfully restored ABT-199 sensitivity in AML cell lines that had developed ABT-199 resistance and increased ABT-199's antileukemic activity in a xenograft model. Mechanistically, the combination of usnic acid and ABT-199 cooperated to boost the expression of the integrated stress response (ISR)-associated genes ATF4, CHOP, and NOXA through the heme-regulated inhibitor kinase (HRI), while also promoting the degradation of the anti-apoptotic protein MCL-1. ISRIB, a compound that blocks the ISR, was able to reverse the growth suppression and cell death, the increase in expression of genes related with the ISR, and the inhibition of MCL-1 protein caused by combination therapy. Additionally, the downregulation of MCL-1 was linked to an increase in MCL-1 phosphorylation at serine 159 and subsequent destruction by the proteasome.

conclusionIn summary, usnic acid improves chemosensitivity to ABT-199 by triggering the integrated stress response, leading to decreased levels of MCL-1 protein, suggesting a potential treatment for AML cases resistant to Bcl-2 inhibitors.

Indexed as

BenzofuransBridged Bicyclo Compounds, HeterocyclicDrug Resistance, NeoplasmLeukemia, Myeloid, AcuteProto-Oncogene Proteins c-bcl-2SulfonamidesAnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell SurvivalHumansMiceXenograft Model Antitumor AssaysAntineoplastic AgentsBCL2 protein, humanBenzofuransBridged Bicyclo Compounds, HeterocyclicProto-Oncogene Proteins c-bcl-2Sulfonamidesusnic acidvenetoclaxABT-199Acute myeloid leukemiaDrug resistanceIntegrated stress responsesMCL-1Usnic acid

Identifiers

PMID39384125
PMCPMC12302291

What Socratic holds

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LicenceCC BY-NC-ND
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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.