胰腺癌
糖酵解
癌症研究
车站3
信号转导
过剩3
肿瘤进展
间质细胞
生物
肿瘤微环境
癌症
细胞生物学
葡萄糖转运蛋白
内分泌学
遗传学
新陈代谢
肿瘤细胞
过剩1
胰岛素
作者
Ziyi Zhong,Kege Yang,Yunlong Li,Shurui Zhou,Hanming Yao,Yue Zhao,Yuzhou Huang,Jinmao Zou,Yaqing Li,Jia Li,Guoda Lian,Kaihong Huang,Shaojie Chen
出处
期刊:Cancer Letters
[Elsevier]
日期:2024-04-01
卷期号:588: 216784-216784
被引量:2
标识
DOI:10.1016/j.canlet.2024.216784
摘要
Glycolytic metabolism is a hallmark of pancreatic ductal adenocarcinoma (PDAC), and tumor-associated stromal cells play important roles in tumor metabolism. We previously reported that tumor-associated macrophages (TAMs) facilitate PDAC progression. However, little is known about whether TAMs are involved in regulating glycolysis in PDAC. Here, we found a positive correlation between CD68+ TAM infiltration and FDG maximal standardized uptake (FDG SUVmax) on PET-CT images of PDAC. We discovered that the glycolytic gene set was prominently enriched in the high TAM infiltration group through Gene Set Enrichment Analysis using The Cancer Genome Atlas database. Mechanistically, TAMs secreted IL-8 to promote GLUT3 expression in PDAC cells, enhancing tumor glycolysis both in vitro and in vivo, whereas this effect could be blocked by the IL-8 receptor inhibitor reparixin. Furthermore, IL-8 promoted the translocation of phosphorylated STAT3 into the nucleus to activate the GLUT3 promoter. Overall, we demonstrated that TAMs boosted PDAC cell glycolysis through the IL-8/STAT3/GLUT3 signaling pathway. Our cumulative findings suggest that the abrogation of TAM-induced tumor glycolysis by reparixin might exhibit an antitumor impact and offer a potential therapeutic target for PDAC.
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