基因敲除
胶质瘤
癌症研究
肿瘤微环境
趋化因子
生物
免疫系统
巨噬细胞极化
小胶质细胞
下调和上调
肿瘤进展
细胞培养
免疫学
体外
炎症
巨噬细胞
癌症
基因
生物化学
遗传学
作者
Jinge Kong,Zhu Mei,Ying Zhang,Luzheng Xu,Jun Zhang,Yun Wang
出处
期刊:Cancer Letters
[Elsevier]
日期:2023-06-09
卷期号:567: 216265-216265
被引量:4
标识
DOI:10.1016/j.canlet.2023.216265
摘要
Gliomas are highly prevalent and aggressive brain tumors. Growing evidence shows that epigenetic changes are closely related to cancer development. Here we report the roles of Chromodomain Y-like (CDYL), an important epigenetic transcriptional corepressor in the central nervous system in glioma progression. We found that CDYL was highly expressed in glioma tissues and cell lines. CDYL knockdown decreased cell mobility in vitro and significantly reduced tumor burden in the xenograft mouse in vivo. RNA sequencing analysis revealed the upregulation of immune pathways after CDYL knockdown, as well as chemokine (C-C motif) ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 12. The immunohistochemistry staining and macrophage polarization assays showed increased infiltration of M1-like tumor-associated macrophages/microglia (TAMs) while decreased infiltration of M2-like TAMs after CDYL knockdown in vivo and in vitro. Following the in situ TAMs depletion or CCL2 antibody neutralization, the tumor-suppressive role of CDYL knockdown was abolished. Collectively, our results show that CDYL knockdown suppresses glioma progression, which is associated with CCL2-recruited monocytes/macrophages and the polarization of M1-like TAMs in the tumor microenvironment, indicating CDYL as a promising target for glioma treatment.
科研通智能强力驱动
Strongly Powered by AbleSci AI