Evidence map›Paper›PMID 42859301›Full record

ArticleMolecular biology reports2026

Hsa_circ_0029325 drives imatinib resistance via the CDCA4/AKT axis in chronic myeloid leukemia.

Xiaoxu Lan, Hang Sun, Yulong Mu, Xiaoqing Hou, Chenhui Ti, Weimiao Sun, Shuyang Xie, Youjie Li, Yunxiao Sun

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Article in Molecular biology 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.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Xiaoxu Lan *Department of Biochemistry and Molecular Biology, Shandong Medical and Pharmaceutical University, 318 Gangcheng East Street, Yantai, 264003, Shandong, P.R. China.
Hang Sun *Shandong Institute of Parasitic Diseases, Shandong First Medical University, Shandong Academy of Medical Sciences, Jining, 272033, Shandong, P.R. China.
Yulong Mu *Department of Biochemistry and Molecular Biology, Shandong Medical and Pharmaceutical University, 318 Gangcheng East Street, Yantai, 264003, Shandong, P.R. China.
Xiaoqing HouDepartment of oral rehabilitation, Yantai Affiliated Hospital of Shandong Medical and Pharmaceutical University, Yantai, 264100, Shandong, P.R. China.
Chenhui TiDepartment of Pediatrics, Yantai Affiliated Hospital of Shandong Medical and Pharmaceutical University, 717 Jinbu Street, Yantai, 264100, Shandong, P.R. China.
Weimiao SunDepartment of Biochemistry and Molecular Biology, Shandong Medical and Pharmaceutical University, 318 Gangcheng East Street, Yantai, 264003, Shandong, P.R. China.
Shuyang XieDepartment of Biochemistry and Molecular Biology, Shandong Medical and Pharmaceutical University, 318 Gangcheng East Street, Yantai, 264003, Shandong, P.R. China.
Youjie LiDepartment of Biochemistry and Molecular Biology, Shandong Medical and Pharmaceutical University, 318 Gangcheng East Street, Yantai, 264003, Shandong, P.R. China. youjie1979@163.com.
Yunxiao SunDepartment of Pediatrics, Yantai Affiliated Hospital of Shandong Medical and Pharmaceutical University, 717 Jinbu Street, Yantai, 264100, Shandong, P.R. China. sunyunxiao1979@163.com.

Funding

Binzhou Medical and Health Science and Technology Project BW20250028National Natural Science Foundation of China 81800169Natural Science Foundation of Shandong Province ZR2022LSW002Natural Science Foundation of Shandong Province ZR2023MH223Shandong Province Medical and Health Technology Development Plan Project 202508011050Yantai Natural Science Foundation ZR2025LZ041
6 · The paper itself

Abstract

backgroundImatinib (IM) resistance poses a major unresolved clinical challenge in chronic myeloid leukemia (CML) treatment, significantly compromising patient prognosis. This study aims to elucidate the role of cell division cycle-associated protein 4 (CDCA4) in IM resistance and the underlying molecular mechanisms in CML. METHODS AND

resultsPan-cancer analysis revealed that high CDCA4 expression was significantly associated with shorter overall survival in multiple cancer types. Quantitative real-time PCR demonstrated upregulated CDCA4 expression in both peripheral blood samples from CML patients and IM-resistant cell lines. CCK-8 assays showed that CDCA4 overexpression markedly enhanced IM resistance and promoted cell proliferation in CML cells. Mechanistic investigations indicated that CDCA4 is associated with hyperactivation of the AKT-mTOR signaling axis and concurrent suppression of basal autophagy, a phenotype that correlates with imatinib chemoresistance in CML cells. Subsequent molecular profiling identified a circ_0029325-dependent regulatory circuit that governs CDCA4 expression levels.

conclusionsOur findings clarify the critical function of CDCA4 in CML IM resistance via the AKT-mTOR/autophagy axis and reveal its upstream circ_0029325 regulatory mechanism. This work provides promising potential biomarkers and therapeutic targets for improving CML treatment outcomes.

Indexed as

Cell Cycle ProteinsDrug Resistance, NeoplasmImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProto-Oncogene Proteins c-aktAntineoplastic AgentsAutophagyCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansSignal TransductionTOR Serine-Threonine KinasesAntineoplastic AgentsCell Cycle ProteinsImatinib MesylateProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKT signaling pathwayCDCA4circ_0029325CMLImatinib-resistance

Identifiers

PMID42859301

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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.