M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy.

IF 4.5 2区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES
iScience Pub Date : 2026-09-30 eCollection Date: 2026-10-16 DOI:10.1016/j.isci.2026.117695
Jiangpeng Fan, Yufei Mao, Li Liu, Zhongyu Ren, Zidong Zhou, Yuanqi Ma, Xiangrong Lu, Guimei Cui, Xu Zhang, Xiuping Zhou
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引用次数: 0

Abstract

Most of glioma patients still experience relapse after radiotherapy owing to the formation of tumor immunosuppressive microenvironment. However, the comprehensive landscape of immune cell infiltration and the molecular mechanisms mediating glioma recurrence remains unclear. Bulk RNA sequencing (RNA-seq) analysis revealed the significant changes in the immune system including increased total tumor-associated macrophages (TAMs) and elevated M2-TAMs in recurrent glioma accepting radiotherapy. Meanwhile, C-C motif chemokine 18 (CCL-18) was the highest elevated molecule after radiotherapy. Consistently, the aforementioned results were confirmed in tissue microarray containing 23 paired gliomas. In vitro, radiation promoted TAM polarization into M2-TAMs, accompanying CCL-18 secretion. However, CCL-18 promoted non-irradiated glioma proliferation but did not mediate glioma recurrence after radiotherapy. Mechanistically, the pro-tumor effect of CCL-18 was weakened by the down-regulation of CCL-18 receptors on glioma accepting radiotherapy. Our study indicates CCL-18 does not mediate glioma recurrence but has the potential to serve as a biomarker for recurrent gliomas.

M2型肿瘤相关巨噬细胞来源的CCL-18促进胶质瘤细胞增殖,但不介导胶质瘤放疗后复发。
由于肿瘤免疫抑制微环境的形成,大多数胶质瘤患者放疗后仍会复发。然而,免疫细胞浸润的综合景观和介导胶质瘤复发的分子机制仍不清楚。大量RNA测序(RNA-seq)分析显示,在接受放疗的复发性胶质瘤中,免疫系统发生了显著变化,包括肿瘤相关巨噬细胞(tam)总量增加和m2 - tam升高。同时,C-C基序趋化因子18 (CCL-18)是放疗后升高最高的分子。同样,上述结果在包含23对胶质瘤的组织微阵列中得到证实。在体外,辐射促进TAM极化成m2 -TAM,并伴随CCL-18分泌。然而,CCL-18促进未辐照胶质瘤增殖,但不介导胶质瘤放疗后复发。机制上,CCL-18受体下调对胶质瘤放疗的促瘤作用减弱。我们的研究表明CCL-18不介导胶质瘤复发,但有可能作为复发胶质瘤的生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
iScience
iScience Multidisciplinary-Multidisciplinary
CiteScore
7.20
自引率
1.70%
发文量
1972
审稿时长
6 weeks
期刊介绍: Science has many big remaining questions. To address them, we will need to work collaboratively and across disciplines. The goal of iScience is to help fuel that type of interdisciplinary thinking. iScience is a new open-access journal from Cell Press that provides a platform for original research in the life, physical, and earth sciences. The primary criterion for publication in iScience is a significant contribution to a relevant field combined with robust results and underlying methodology. The advances appearing in iScience include both fundamental and applied investigations across this interdisciplinary range of topic areas. To support transparency in scientific investigation, we are happy to consider replication studies and papers that describe negative results. We know you want your work to be published quickly and to be widely visible within your community and beyond. With the strong international reputation of Cell Press behind it, publication in iScience will help your work garner the attention and recognition it merits. Like all Cell Press journals, iScience prioritizes rapid publication. Our editorial team pays special attention to high-quality author service and to efficient, clear-cut decisions based on the information available within the manuscript. iScience taps into the expertise across Cell Press journals and selected partners to inform our editorial decisions and help publish your science in a timely and seamless way.
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