ANP32B suppresses B‐cell acute lymphoblastic leukemia through activation of PU.1 in mice

Author:

Yang Qian1,Liu Hao‐Ran1,Yang Shuo2,Wei Yu‐Sheng1,Zhu Xiao‐Na3,Zhi Zhe3,Zhu Di3,Chen Guo‐Qiang3,Yu Yun3ORCID

Affiliation:

1. Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui‐Jin Hospital Shanghai Jiao‐Tong University School of Medicine (SJTU‐SM) Shanghai China

2. Department of Laboratory Medicine, Zhongshan Hospital Fudan University Shanghai China

3. Institute of Aging & Tissue Regeneration, State Key Laboratory of Oncogenes and Related Genes and Chinese Academy of Medical Sciences Research Unit (NO.2019RU043), Ren‐Ji Hospital Shanghai Jiao‐Tong University School of Medicine (SJTU‐SM) Shanghai China

Abstract

AbstractANP32B, a member of the acidic leucine‐rich nuclear phosphoprotein 32 kDa (ANP32) family of proteins, is critical for normal development because its constitutive knockout mice are perinatal lethal. It is also shown that ANP32B acts as a tumor‐promoting gene in some kinds of cancer such as breast cancer and chronic myelogenous leukemia. Herein, we observe that ANP32B is lowly expressed in B‐cell acute lymphoblastic leukemia (B‐ALL) patients, which correlates with poor prognosis. Furthermore, we utilized the N‐myc or BCR‐ABLp190‐induced B‐ALL mouse model to investigate the role of ANP32B in B‐ALL development. Intriguingly, conditional deletion of Anp32b in hematopoietic cells significantly promotes leukemogenesis in two B‐ALL mouse models. Mechanistically, ANP32B interacts with purine rich box‐1 (PU.1) and enhances the transcriptional activity of PU.1 in B‐ALL cells. Overexpression of PU.1 dramatically suppresses B‐ALL progression, and highly expressed PU.1 significantly reverses the accelerated leukemogenesis in Anp32b‐deficient mice. Collectively, our findings identify ANP32B as a suppressor gene and provide novel insight into B‐ALL pathogenesis.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cancer Research,Oncology,General Medicine

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