白血病是一组克隆性造血干祖细胞的恶性疾病,其病理机制尚待阐明。遗传和表观遗传异常,以及微环境因素,包括细胞因子,在白血病发生中起关键作用。巨噬细胞迁移抑制因子(MIF)已被认为是肿瘤发生的关键调节因子之一。血管生成和肿瘤转移。本文主要探讨MIF及其通路在肿瘤中的功能作用,尤其是白血病。MIF/CD74相互作用在肿瘤细胞存活中起着重要作用,例如上调BCL‑2和CD84表达,和激活受体型酪氨酸磷酸酶ζ。此外,MIF上调响应缺氧诱导因子形成促肿瘤微环境,并促进促炎细胞因子的产生。此外,MIF启动子序列的多态性与白血病的发展有关。MIF信号靶向的早期临床试验显示出积极的结果。总的来说,这些努力为白血病的干预提供了有希望的手段.
Leukemia is a group of malignant diseases of clonal hematopoietic stem‑progenitor cells and its pathological mechanisms remain to be elucidated. Genetic and epigenetic abnormalities, as well as microenvironmental factors, including cytokines, serve critical roles in leukaemogenesis. Macrophage migration inhibitory factor (MIF) has been presented as one of the key regulators in tumorigenesis, angiogenesis and tumor metastasis. This article focuses on the functional role of
MIF and its pathway in cancer, particularly in leukemia.
MIF/CD74 interaction serves prominent roles in tumor cell survival, such as upregulating BCL‑2 and CD84 expression, and activating receptor‑type tyrosine phosphatase ζ. Furthermore,
MIF upregulation forms a pro‑tumor microenvironment in response to hypoxia‑induced factors and promotes pro‑inflammatory cytokine production. Additionally, polymorphisms of the
MIF promoter sequence are associated with leukemia development.
MIF signal‑targeted early clinical trials show positive results. Overall, these efforts provide a promising means for intervention in leukemia.