KIF2C通过调节STAT3/IL-10轴来调节巨细胞M2极化和DLBCL进展
Li Qian1, Rongfeng Shi2, Juanjuan Yang1
1Department of Pathology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
Cellular signalling
|October 2, 2025
概括
素家族成员2C (KIF2C) 通过激活STAT3/IL-10通路,促进M2巨分离和瘤进展在扩散型大B细胞淋巴瘤 (DLBCL) 中. 准KIF2C为DLBCL提供了一个潜在的治疗策略.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 素家族成员2C (KIF2C) 是一种瘤基因,与各种癌症有关.
- 它在扩散性大B细胞淋巴瘤 (DLBCL) 中的特定作用及其与瘤微环境组件 (如巨细胞) 的相互作用尚未得到充分了解.
研究的目的:
- 研究KIF2C在DLBCL中的功能,重点关注其在巨细胞极化和瘤进展中的作用.
- 阐明涉及STAT3/IL-10信号通路的潜在分子机制.
主要方法:
- 使用DLBCL细胞系 (OCI-LY3) 条件介质,将THP-1细胞分化为M0,M1和M2巨细胞.
- 在THP-1和OCI-LY3细胞中操纵了KIF2C表达 (敲击/过度表达).
- 进行了共同培养实验和体外/体内测试 (增殖,迁移,入侵,亡,异种移植模型).
- 西方涂抹用于评估p-STAT3水平,并应用STAT3激动剂来评估IL-10表达和M2极化.
主要成果:
- 在M2巨细胞极化过程中,KIF2C表达被上调.
- KIF2C促进了M2极化,并增强了DLBCL细胞的增殖,迁移和入侵.
- 通过KIF2C Knockdown降低了p-STAT3水平,IL-10表达和M2极化,这些效应通过STAT3激活部分恢复.
- 在体内,KIF2C敲击抑制了瘤生长,M2极化和IL-10表达.
结论:
- 在DLBCL中,KIF2C在促进M2巨分化和促进瘤的行为方面发挥着重要作用.
- 由KIF2C介导的STAT3/IL-10轴对于调节瘤微环境和DLBCL进展至关重要.
- 在DLBCL治疗中,KIF2C是一个有前途的治疗标.
相关概念视频
The JAK-STAT Signaling Pathway
12.1K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
12.1K
T Cell Types and Functions
2.2K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.2K
Receptor Downregulation in MVBs
2.8K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
2.8K
TGF - β Signaling Pathway
10.5K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.5K


