Extracellular matrix

Friedman, Scott L.

doi:10.1002/9781118663387.ch6

Cited by 2 publications

(2 citation statements)

References 121 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hepatic ECM consists of 20 genetically distinct types of collagen, noncollagenous glycoproteins such as elastin, laminin, and fibronectin; proteoglycans such as aggrecan, fibromodulin, decorin, biglycan, glypicans, and syndecans; as well as matricellular proteins such as thrombospondins, osteopontin, tenascins, the CCN family of proteins, and connective tissue growth factor (CTGF). Many of these ECM proteins change during liver fibrosis (39). …”

Section: Hepatocellular Carcinomamentioning

confidence: 99%

“…DDR2 is expressed not only on fibrogenic cells, promoting a positive feedback loop for their activation (41) but also in the epithelial compartment to promote the epithelial-mesenchymal transition (EMT; 42, 43), a key mechanism contributing to the malignant transformation of epithelia. Moreover, ECM proteins, including decorin, biglycan, fibromodulin, and glycosaminoglycans, store growth factors such as HGF, PDGF, TGF-β, CTGF, and VEGF (39). ECM turnover during fibrogenesis and fibrosis resolution results in liberation and activation of growth factor signaling cascades, promoting epithelial proliferation and, most likely, cancer development in chronically injured livers.…”

Section: Hepatocellular Carcinomamentioning

confidence: 99%

See 1 more Smart Citation

The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer

Affò

Schwabe

2017

Annu. Rev. Pathol. Mech. Dis.

502

425

View full text Add to dashboard Cite

Liver cancer is the second leading cause of cancer mortality worldwide, causing more than 700,000 deaths annually. Because of the wide landscape of genomic alterations and limited therapeutic success of targeting tumor cells, a recent focus has been on better understanding and possibly targeting the microenvironment in which liver tumors develop. A unique feature of liver cancer is its close association with liver fibrosis. More than 80% of hepatocellular carcinomas (HCCs) develop in fibrotic or cirrhotic livers, suggesting an important role of liver fibrosis in the premalignant environment (PME) of the liver. Cholangiocarcinoma (CCA), in contrast, is characterized by a strong desmoplasia that typically occurs in response to the tumor, suggesting a key role of cancer-associated fibroblasts (CAFs) and fibrosis in its tumor microenvironment (TME). Here, we discuss the functional contributions of myofibroblasts, CAFs, and fibrosis to the development of HCC and CCA in the hepatic PME and TME, focusing on myofibroblast- and extracellular matrix—associated growth factors, fibrosis-associated immunosuppressive pathways, as well as mechanosensitive signaling cascades that are activated by increased tissue stiffness. Better understanding of the role of myofibroblasts in HCC and CCA development and progression may provide the basis to target these cells for tumor prevention or therapy.

show abstract

Section: Hepatocellular Carcinomamentioning

confidence: 99%

Section: Hepatocellular Carcinomamentioning

confidence: 99%