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Biomedicines
Volume 13
Issue 2
10.3390/biomedicines13020292
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Article

β-Catenin Regulates Glycolytic and Mitochondrial Function in T-Cell Acute Lymphoblastic Leukemia

by
Ling Zhang
1,†,
Yu Zhao
2,†,
Shuoting Wang
1,
Jian Zhang
3,
Xiaohui Li
1,
Shuangyin Wang
2,
Taosheng Huang
4,
Jinxing Wang
5,* and
Jiajun Liu
1,*
1
Department of Hematology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China
2
Department of Hematology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China
3
Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China
4
The Medicine and Biological Engineering Technology Research Center of the Ministry of Health, Guangzhou 510663, China
5
Department of Pathology Technique, Guangdong Medical University, Dongguan 523808, China
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Biomedicines 2025, 13(2), 292; https://doi.org/10.3390/biomedicines13020292
Submission received: 5 January 2025 / Revised: 17 January 2025 / Accepted: 21 January 2025 / Published: 24 January 2025
(This article belongs to the Special Issue Innovative Approaches to Molecular Pathogenesis and Therapy of Lymphoid Malignancies)
Versions Notes

Abstract

Background: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy characterized by a poor prognosis. β-catenin is implicated in the progression of T-ALL, yet the precise mechanisms of β-catenin involvement in the pathogenesis of T-ALL, particularly concerning metabolic processes, remain inadequately elucidated. Methods: A β-catenin knockout cell line was generated in the human leukemic cell line Jurkat using the CRISPR-Cas9 technique. Subsequently, assays were performed to evaluate cell proliferation, apoptosis, and metabolic activity. Comparative transcriptomic analysis was conducted between control cells and β-catenin knockout cells. Finally, a mouse xenograft model was employed to assess whether β-catenin knockout attenuates tumor growth and infiltration in vivo. Results: The deletion of β-catenin significantly inhibited proliferation and induced apoptosis. Additionally, the silencing of β-catenin led to the inhibition of glycolysis and a reduction in both mitochondrial mass and membrane potential. These results indicate that β-catenin may play a crucial role in regulating cell proliferation and apoptosis through the modulation of glycolytic activity and mitochondrial function in T-ALL. Conclusions: In summary, our findings uncover a novel mechanism by which β-catenin influences glycolysis and mitochondrial function in the progression of T-ALL, thereby identifying a potential therapeutic target for patients with relapsed T-ALL.
Keywords: β-catenin; T-cell acute lymphoblastic leukemia; glycolysis; mitochondrial function β-catenin; T-cell acute lymphoblastic leukemia; glycolysis; mitochondrial function

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MDPI and ACS Style

Zhang, L.; Zhao, Y.; Wang, S.; Zhang, J.; Li, X.; Wang, S.; Huang, T.; Wang, J.; Liu, J. β-Catenin Regulates Glycolytic and Mitochondrial Function in T-Cell Acute Lymphoblastic Leukemia. Biomedicines 2025, 13, 292. https://doi.org/10.3390/biomedicines13020292

AMA Style

Zhang L, Zhao Y, Wang S, Zhang J, Li X, Wang S, Huang T, Wang J, Liu J. β-Catenin Regulates Glycolytic and Mitochondrial Function in T-Cell Acute Lymphoblastic Leukemia. Biomedicines. 2025; 13(2):292. https://doi.org/10.3390/biomedicines13020292

Chicago/Turabian Style

Zhang, Ling, Yu Zhao, Shuoting Wang, Jian Zhang, Xiaohui Li, Shuangyin Wang, Taosheng Huang, Jinxing Wang, and Jiajun Liu. 2025. "β-Catenin Regulates Glycolytic and Mitochondrial Function in T-Cell Acute Lymphoblastic Leukemia" Biomedicines 13, no. 2: 292. https://doi.org/10.3390/biomedicines13020292

APA Style

Zhang, L., Zhao, Y., Wang, S., Zhang, J., Li, X., Wang, S., Huang, T., Wang, J., & Liu, J. (2025). β-Catenin Regulates Glycolytic and Mitochondrial Function in T-Cell Acute Lymphoblastic Leukemia. Biomedicines, 13(2), 292. https://doi.org/10.3390/biomedicines13020292

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