巨噬细胞通过趋化因子和细胞因子信号指导结肠癌中的异常糖基化。

Macrophages Instruct Aberrant Glycosylation in Colon Cancer by Chemokine and Cytokine Signals.

机构信息

Department of Medicine of Verona University, Verona, Italy.

出版信息

Cancer Immunol Res. 2020 Feb;8(2):160. doi: 10.1158/2326-6066.CIR-19-1005.

PMID:32015012

Abstract

Myeloid cells can alter diverse molecular and metabolic pathways in cancer cells, contributing to their survival, migration, and resistance to chemotherapy and immune attack. The results by Kvorjak and colleagues unveil a novel circuit whereby altered glycosylation in epithelial cells promotes the pathogenesis of ulcerative colitis and colitis-associated colon cancer, via the production of IL13 and CCL17 by M2-polarized macrophages..

摘要

髓样细胞可以改变癌细胞中的多种分子和代谢途径，促进其存活、迁移以及对化疗和免疫攻击的抵抗。Kvorjak 及其同事的研究结果揭示了一个新的途径，即上皮细胞中糖基化的改变通过 M2 极化的巨噬细胞产生 IL13 和 CCL17，促进溃疡性结肠炎和结肠炎相关结肠癌的发病机制。