期刊
CANCERS
卷 11, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/cancers11030290
关键词
pancreatic cancer; PDAC; cancer-associated fibroblast; myofibroblast; inflammation; IL-6; CXCL8; TGF-beta
类别
资金
- National Cancer Institute, National Institutes of Health [U54CA163120, R01CA228524]
- Cancer Center Support Grant from the National Cancer Institute, National Institutes of Health [P30CA036727]
- King Fahad Specialist Hospital-Dammam
- Saudi Arabian Cultural mission in the USA
- University of Nebraska Medical Center
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related deaths in the USA. Desmoplasia and inflammation are two major hallmarks of PDAC. Desmoplasia, composed of extracellular matrix (ECM), cancer-associated fibroblasts (CAFs), and infiltrating immune and endothelial cells, acts as a biophysical barrier to hinder chemotherapy and actively contributes to tumor progression and metastasis. CAFs represent a multifunctional subset of PDAC microenvironment and contribute to tumor initiation and progression through ECM deposition and remodeling, as well as the secretion of paracrine factors. Attempts to resolve desmoplasia by targeting CAFs can render an adverse outcome, which is likely due to CAFs heterogeneity. Recent reports describe subsets of CAFs that assume more secretory functions, in addition to the typical myofibroblast phenotype. Here, we review the literature and describe the relationship between CAFs and inflammation and the role of the secretory-CAFs in PDAC.
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