关键词: CXCL3 CXCR2 Carcinogenesis Inflammation Tumor microenvironment

Mesh : Humans Tumor Microenvironment Inflammation / metabolism Animals Chemokines, CXC / metabolism Neoplasms / metabolism pathology Signal Transduction Carcinogenesis / metabolism

来  源:   DOI:10.1016/j.lfs.2024.122691

Abstract:
CXCL3 (C-X-C Motif Chemokine 3), a member of the C-X-C chemokine subfamily, operates as a potent chemoattractant for neutrophils, thereby orchestrating the recruitment and migration of leukocytes alongside eliciting an inflammatory response. Recent inquiries have shed light on the pivotal roles of CXCL3 in the context of carcinogenesis. In the tumor microenvironment, CXCL3 emanating from both tumor and stromal cells intricately modulates cellular behaviors through autocrine and paracrine actions, primarily via interaction with its receptor CXCR2. Activation of signaling cascades such as ERK/MAPK, AKT, and JAK2/STAT3 underscores CXCL3\'s propensity to favor tumorigenic processes. However, CXCL3 exhibits dualistic behaviors, as evidenced by its capacity to exert anti-tumor effects under specific conditions. Additionally, the involvement of CXCL3 extends to inflammatory disorders like eclampsia, obesity, and asthma. This review encapsulates the structural attributes, biological functionalities, and molecular underpinnings of CXCL3 across both tumorigenesis and inflammatory diseases.
摘要:
CXCL3(C-X-C基序趋化因子3),C-X-C趋化因子亚家族的一员,作为嗜中性粒细胞的有效化学引诱物,从而协调白细胞的募集和迁移,同时引发炎症反应。最近的调查揭示了CXCL3在致癌作用中的关键作用。在肿瘤微环境中,来自肿瘤和基质细胞的CXCL3通过自分泌和旁分泌作用复杂地调节细胞行为。主要通过与其受体CXCR2的相互作用。激活信号级联,如ERK/MAPK,AKT,JAK2/STAT3强调CXCL3倾向于肿瘤形成过程。然而,CXCL3表现出二元行为,其在特定条件下发挥抗肿瘤作用的能力证明了这一点。此外,CXCL3的参与延伸到炎症性疾病如子痫,肥胖,和哮喘。这篇评论概括了结构属性,生物功能,以及CXCL3在肿瘤发生和炎症性疾病中的分子基础。
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