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USP1 promotes the aerobic glycolysis and progression of T-cell acute lymphoblastic leukemia via PLK1/LDHA axis

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机构： [1]Beijing Children's Hospital, Beijing, China. [2]Children's Hospital of Fudan University, Shanghai, China. [3]Shanghai Cancer Institute, Shanghai, China. [4]Beijing Children's Hospital, Capital Medical University. [5]Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China. [6]Fudan University, Shanghai, China. [7]Beijing Children's Hospital of Capital Medical University, Beijing, China. [8]Quzhou People's Hospital, Quzhou, China. [9]West China Hospital, Sichuan University, Chengdu, China. [10]Children's Hospital of Fudan University, Shang Hai, China. [11]Shanghai Children's Medical Center, Shanghai, China.

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The effect of aerobic glycolysis remains elusive in pediatric acute T lymphoblastic leukemia (T-ALL). Increasing evidence has revealed that dysregulation of deubiquitination is involved in glycolysis, by targeting glycolytic rate-limiting enzymes. Here, we demonstrated that upregulated deubiquitinase USP1 expression correlated with poor prognosis in pediatric primary T-ALL samples. USP1 depletion abolished cellular proliferation and attenuated glycolytic metabolism. In vivo experiments showed that USP1 suppression decreased leukemia progression in nude mice. Inhibition of USP1 caused a decrease of both mRNA and protein levels in LDHA, a critical glycolytic enzyme. Moreover, USP1 interacted with and deubiquitinated PLK1, a critical regulator of glycolysis. Overexpression of USP1 with upregulated PLK1 was observed in most T-ALL patient samples. In addition, PLK1 inhibition reduced LDHA expression and abrogated the USP1-mediated increase of cell proliferation and lactate level. Ectopic expression of LDHA can rescue the suppressive effect of USP1 silencing on cell growth and lactate production. Pharmacological inhibition of USP1 by ML323 exhibited cell cytotoxicity in human T-ALL cells. Taken together, our results demonstrated that USP1 may be a promising therapeutic target in pediatric T-ALL.Copyright © 2023 American Society of Hematology.

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出版当年[2023]版：

大类 | 1 区

医学

小类 | 2 区血液学

最新[2023]版：

大类 | 1 区

医学

小类 | 2 区血液学

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出版当年[2023]版：

Q1 HEMATOLOGY

最新[2023]版：

Q1 HEMATOLOGY

影响因子： 7.4 最新[2023版] 7.2 最新五年平均 7.4 出版当年[2023版] 7.2 出版当年五年平均 7.6 出版前一年[2022版]

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第一作者机构： [1]Beijing Children's Hospital, Beijing, China.

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