期刊
BIOCHEMICAL JOURNAL
卷 441, 期 -, 页码 541-552出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20111240
关键词
chemoresistance; fibrosis; microRNA; membrane-type 1 matrix metalloproteinase (MT1-MMP); pancreatic cancer; Snail; transforming growth factor-beta (TGF-beta)
资金
- National Institutes of Health/National Cancer Institute [R01CA126888, U54CA151880]
PDAC (pancreatic ductal adenocarcinoma) is among the most deadly of human malignances. A hallmark of the disease is a pronounced collagen-rich fibrotic extracellular matrix known as the desmoplastic reaction. Intriguingly, it is precisely these areas of fibrosis in which human PDAC tumours demonstrate increased expression of a key collagenase, MT1-MMP [membrane-type 1 MMP (matrix metalloproteinase); also known as MMP-14]. Furthermore, a cytokine known to mediate fibrosis in vivo, TGF-beta 1 (transforming growth factor-beta 1), is up-regulated in human PDAC tumours and can promote MT1-MMP expression. In the present review, we examine the regulation of PDAC progression through the interplay between type I collagen (the most common extracellular matrix present in human PDAC tumours), MT1-MMP and TGF-beta 1. Specifically, we examine the way in which signalling events through these pathways mediates invasion, regulates microRNAs and contributes to chemoresistance.
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