[Expression and Clinical Significance of CaMKIIγ in Patients with Acute Myeloid Leukemia].

Zhongguo Shi Yan Xue Ye Xue Za Zhi

Department of Laboratory Medicine, The First Affiliated Hospital of Shihezi University, Shihezi 832008, Xinjiang Uygur Autonomous Region, China.

Published: June 2025


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Article Abstract

Objective: To investigate the expression and potential mechanism of calcium/calmodulin-dependent protein kinase II gamma (CaMKIIγ) in patients with acute myeloid leukemia (AML).

Methods: Peripheral blood samples were collected from 90 AML patients, and mononuclear cells were isolated. The expression of CaMKIIγ was measured using real-time quantitative PCR and Western blot. The diagnostic value of CaMKIIγ for AML was assessed, and its correlation with clinical characteristics was analyzed using the clinical data of patients. Additionally, the molecular mechanisms of CaMKIIγ were preliminarily explored.

Results: Compared with the control group, the expression of was significantly upregulated in AML patients. Receiver operating characteristic (ROC) curve analysis showed that could serve as a promising biomarker for distinguishing AML patients from healthy individuals. Furthermore, was significantly correlated with white blood cell (WBC) count and mutation. CaMKIIγ was highly expressed in both newly diagnosed and relapsed AML patients, while decreased during remission. In AML cell lines, the expression levels of CaMKIIγ were all elevated. Inhibition of phosphorylated CaMKIIγ by berbamine led to a decrease in pAKT and pSTAT5 expression.

Conclusion: CaMKIIγ is significantly upregulated in AML patients, and is associated with poor clinicopathological features and unfavorable prognosis. It may serve as a prognostic marker and potential therapeutic target in AML. Its expression may be related to the activation of pAKT and pSTAT5, suggesting that CaMKIIγ may contribute to the development and progression of AML through the activation of the AKT/STAT5 signaling pathway.

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http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2025.03.015DOI Listing

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