1. Academic Validation
  2. CD93 promotes acute myeloid leukemia development and is a potential therapeutic target

CD93 promotes acute myeloid leukemia development and is a potential therapeutic target

  • Exp Cell Res. 2022 Nov 15;420(2):113361. doi: 10.1016/j.yexcr.2022.113361.
Jie Jia 1 Bin Liu 2 Dandan Wang 1 Xiaohong Wang 1 Lingrui Song 1 Yanzhang Ren 1 Zhaoming Guo 1 Kun Ma 1 Changhao Cui 3
Affiliations

Affiliations

  • 1 School of Life and Pharmaceutical Sciences, Dalian University of Technology, Panjin, 124221, China.
  • 2 Cancer Hospital of Dalian University of Technology, Liaoning Cancer Hospital & Institute, Shenyang, 110042, China.
  • 3 School of Life and Pharmaceutical Sciences, Dalian University of Technology, Panjin, 124221, China. Electronic address: [email protected].
Abstract

CD93 is a transmembrane receptor belonging to the Group XIV C-Type lectin family. It is expressed in a variety of cellular types such as monocytes, neutrophils, platelets, microglia, and endothelial cells. CD93 has been reported to play important roles in cell proliferation, cell migration, and tumor angiogenesis. Here, we show CD93 is highly expressed in M4 and M5 subtypes of acute myeloid leukemia (AML) patients, and highly expressed in leukemia stem cells, AML progenitor cells, as well as more differentiated AML cells. We found that CD93 promotes AML cell proliferation, while CD93 deficient AML cells commit to differentiation. We further show that CD93 exerts its proliferative function through downstream SHP-2/Syk/CREB cascade in AML cells. Moreover, human AML cells treated with CD93 mAb combined with αMFc-NC-DM1 (an IgG Fc specific antibody conjugated to maytansinoid DM1), showed a striking reduction of proliferation. Our study revealed that CD93 is a critical participator of AML development and provides a potential therapeutic cell surface target. (160 words).

Keywords

Acute myeloid leukemia; CD93; CD93 mAb; SHP-2/Syk/CREB cascade.

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  • HY-100388
    99.80%, SHP2 Inhibitor