Expression and Clinical Significance of CaMKIIγ in Patients with Acute Myeloid Leukemia.
10.19746/j.cnki.issn.1009-2137.2025.03.015
- Author:
Ming-Kai LIU
1
;
Xu DAI
1
;
Xiao-Ying ZHAO
1
;
Wei-Wei ZHENG
2
;
Ya-Jing MA
1
Author Information
1. Department of Laboratory Medicine, The First Affiliated Hospital of Shihezi University, Shihezi 832008, Xinjiang Uygur Autonomous Region, China.
2. Department of Laboratory Medicine, The First Affiliated Hospital of University of Science and Technology of China, Hefei 230001, Anhui Province, China.
- Publication Type:Journal Article
- Keywords:
acute myeloid leukemia;
CaMKIIγ
- MeSH:
Humans;
Leukemia, Myeloid, Acute/metabolism*;
Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism*;
STAT5 Transcription Factor/metabolism*;
Male;
Female;
Proto-Oncogene Proteins c-akt/metabolism*;
Mutation;
Middle Aged;
Adult;
Clinical Relevance
- From:
Journal of Experimental Hematology
2025;33(3):726-732
- CountryChina
- Language:Chinese
-
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 CaMKIIγ was significantly upregulated in AML patients. Receiver operating characteristic (ROC) curve analysis showed that CaMKIIγ could serve as a promising biomarker for distinguishing AML patients from healthy individuals. Furthermore, CaMKIIγ was significantly correlated with white blood cell (WBC) count and FLT3-ITD 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.
