文章：

CXCR1、CXCR2、CXCR3、CXCR5及CXCR6配体在急性髓系白血病分子机制与临床诊疗中的作用

The Role of CXCR1, CXCR2, CXCR3, CXCR5, and CXCR6 Ligands in Molecular Cancer Processes and Clinical Aspects of Acute Myeloid Leukemia (AML)

原文发布日期：14 September 2023

DOI: 10.3390/cancers15184555

类型: Article

开放获取: 是

英文摘要：

Acute myeloid leukemia (AML) is a type of leukemia known for its unfavorable prognoses, prompting research efforts to discover new therapeutic targets. One area of investigation involves examining extracellular factors, particularly CXC chemokines. While CXCL12 (SDF-1) and its receptor CXCR4 have been extensively studied, research on other CXC chemokine axes in AML is less developed. This study aims to bridge that gap by providing an overview of the significance of CXC chemokines other than CXCL12 (CXCR1, CXCR2, CXCR3, CXCR5, and CXCR6 ligands and CXCL14 and CXCL17) in AML’s oncogenic processes. We explore the roles of all CXC chemokines other than CXCL12, in particular CXCL1 (Gro-α), CXCL8 (IL-8), CXCL10 (IP-10), and CXCL11 (I-TAC) in AML tumor processes, including their impact on AML cell proliferation, bone marrow angiogenesis, interaction with non-leukemic cells like MSCs and osteoblasts, and their clinical relevance. We delve into how they influence prognosis, association with extramedullary AML, induction of chemoresistance, effects on bone marrow microvessel density, and their connection to French–American–British (FAB) classification and FLT3 gene mutations.

摘要翻译： 

急性髓系白血病（AML）是一种预后不良的白血病类型，这促使研究界致力于探索新的治疗靶点。其中一个研究方向涉及细胞外因子，特别是CXC趋化因子。尽管CXCL12（SDF-1）及其受体CXCR4已被广泛研究，但针对AML中其他CXC趋化因子轴的研究尚不充分。本研究旨在填补这一空白，系统综述除CXCL12外的CXC趋化因子（包括CXCR1、CXCR2、CXCR3、CXCR5和CXCR6的配体，以及CXCL14和CXCL17）在AML致癌过程中的作用。我们重点探讨除CXCL12外的所有CXC趋化因子，特别是CXCL1（Gro-α）、CXCL8（IL-8）、CXCL10（IP-10）和CXCL11（I-TAC）在AML肿瘤进程中的功能，包括它们对AML细胞增殖、骨髓血管生成、与间充质干细胞和成骨细胞等非白血病细胞的相互作用及其临床意义。我们深入分析这些趋化因子如何影响AML预后、与髓外AML的关联、诱导化疗耐药性、对骨髓微血管密度的作用，以及它们与法美英（FAB）分型和FLT3基因突变的相关性。

原文链接：

The Role of CXCR1, CXCR2, CXCR3, CXCR5, and CXCR6 Ligands in Molecular Cancer Processes and Clinical Aspects of Acute Myeloid Leukemia (AML)