促炎细胞因子
生物
癌症研究
白血病
造血
髓系白血病
上睑下垂
免疫系统
免疫学
细胞生物学
炎症
干细胞
炎症体
作者
Julie Mondet,Simon Chevalier,Pascal Mossuz
出处
期刊:Molecules
[MDPI AG]
日期:2021-03-02
卷期号:26 (5): 1323-1323
被引量:17
标识
DOI:10.3390/molecules26051323
摘要
Deregulations of the expression of the S100A8 and S100A9 genes and/or proteins, as well as changes in their plasma levels or their levels of secretion in the bone marrow microenvironment, are frequently observed in acute myeloblastic leukemias (AML) and acute lymphoblastic leukemias (ALL). These deregulations impact the prognosis of patients through various mechanisms of cellular or extracellular regulation of the viability of leukemic cells. In particular, S100A8 and S100A9 in monomeric, homodimeric, or heterodimeric forms are able to modulate the survival and the sensitivity to chemotherapy of leukemic clones through their action on the regulation of intracellular calcium, on oxidative stress, on the activation of apoptosis, and thanks to their implications, on cell death regulation by autophagy and pyroptosis. Moreover, biologic effects of S100A8/9 via both TLR4 and RAGE on hematopoietic stem cells contribute to the selection and expansion of leukemic clones by excretion of proinflammatory cytokines and/or immune regulation. Hence, the therapeutic targeting of S100A8 and S100A9 appears to be a promising way to improve treatment efficiency in acute leukemias.
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