核梭杆菌
自分泌信号
旁分泌信号
癌症研究
间质细胞
胰腺癌
生物
免疫系统
癌细胞
细胞因子
免疫学
癌症
细胞培养
受体
生物化学
遗传学
牙龈卟啉单胞菌
细菌
作者
Barath Udayasuryan,Raffae N. Ahmad,Tam T. D. Nguyen,Ariana Umaña,LaDeidra Monét Roberts,Polina Sobol,Stephen D. Jones,Jennifer M. Munson,Daniel J. Slade,Scott S. Verbridge
出处
期刊:Science Signaling
[American Association for the Advancement of Science (AAAS)]
日期:2022-10-18
卷期号:15 (756)
被引量:55
标识
DOI:10.1126/scisignal.abn4948
摘要
The tumor microbiome is increasingly implicated in cancer progression and resistance to chemotherapy. In pancreatic ductal adenocarcinoma (PDAC), high intratumoral loads of Fusobacterium nucleatum correlate with shorter survival in patients. Here, we investigated the potential mechanisms underlying this association. We found that F. nucleatum infection induced both normal pancreatic epithelial cells and PDAC cells to secrete increased amounts of the cytokines GM-CSF, CXCL1, IL-8, and MIP-3α. These cytokines increased proliferation, migration, and invasive cell motility in both infected and noninfected PDAC cells but not in noncancerous pancreatic epithelial cells, suggesting autocrine and paracrine signaling to PDAC cells. This phenomenon occurred in response to Fusobacterium infection regardless of the strain and in the absence of immune and other stromal cells. Blocking GM-CSF signaling markedly limited proliferative gains after infection. Thus, F. nucleatum infection in the pancreas elicits cytokine secretion from both normal and cancerous cells that promotes phenotypes in PDAC cells associated with tumor progression. The findings support the importance of exploring host-microbe interactions in pancreatic cancer to guide future therapeutic interventions.
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