Evidence map›Paper›PMID 40583859›Full record

ArticleBiophysics reviews2025

The drug resistance feature of acute myeloid leukemia is related to the cell stiffness.

Yu Wang, Hao Jiang, Zhenwei Su, Ran Wang, Xinyuan Luo, Lingxiao Zhang, Zhi Ping Xu, Fenfang Li, Chao He

Abstract read
In one paragraph

Article in Biophysics reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Yu WangInstitute of Chemical Biology, Shenzhen Bay Laboratory, Shenzhen 518107, China.
Hao JiangInstitute of Biomedical Engineering, Shenzhen Bay Laboratory, Shenzhen 518132, People's Republic of China.ORCID https://orcid.org/0009-0007-2504-8747
Zhenwei SuInstitute of Chemical Biology, Shenzhen Bay Laboratory, Shenzhen 518107, China.ORCID https://orcid.org/0000-0002-4832-4122
Ran WangInstitute of Chemical Biology, Shenzhen Bay Laboratory, Shenzhen 518107, China.ORCID https://orcid.org/0000-0002-1741-6446
Xinyuan LuoInstitute of Biomedical Engineering, Shenzhen Bay Laboratory, Shenzhen 518132, People's Republic of China.ORCID https://orcid.org/0009-0004-5093-2081
Lingxiao ZhangInterdisciplinary Nanoscience Center (INANO), Aarhus University, Aarhus C DK-8000, Denmark.ORCID https://orcid.org/0000-0002-7066-6065
Fenfang LiInstitute of Biomedical Engineering, Shenzhen Bay Laboratory, Shenzhen 518132, People's Republic of China.ORCID https://orcid.org/0000-0002-1690-3373
Chao HeInstitute of Chemical Biology, Shenzhen Bay Laboratory, Shenzhen 518107, China.ORCID https://orcid.org/0000-0002-6224-3484

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a hematologic cancer. Cytarabine-based chemotherapy is the primary treatment. However, drug resistance presents a significant challenge leading to treatment failure. Our study explores the underlying correlation between AML stiffness and its drug resistance feature. We employed microfluidic technology to measure AML cell deformability, demonstrating that drug-resistant cells exhibit increased stiffness compared to their drug-sensitive counterparts. Transcriptomic analysis revealed that enhanced stiffness in drug-resistant cells is associated with upregulated cytoskeletal protein expression and increased lipid metabolism, particularly the peroxisome proliferators-activated receptor (PPAR) signaling pathway. Mechanistically, we found that knocking down PLIN2 at the genetic level and increasing the cholesterol level promoted the deformation of drug-resistant cells, indicating that intracellular lipid levels are involved in the regulation of cell softness. Our findings suggest that AML cell stiffness could serve as a potential biomarker for drug resistance, providing new insights into the mechanisms underlying AML drug resistance and offering potential therapeutic targets.

Identifiers

PMID40583859
PMCPMC12201995

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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.