الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
subunit of integrin, with small interfering RNA, reduced stimulation of tumor proliferation and invasion by periostin (Utispan et al., 2010). The ECM that surrounds pancreatic tumors also has been shown to overexpress periostin, which promotes tumor invasiveness (Utispan et al., 2007). Tenascin-C, another ECM protein produced by CAFs, also promotes tumor migration and invasiveness (Sirica, 2012). In CCA cell lines, HGF promoted invasiveness and motility by inducing phosphorylation of Akt and ERK 1/2 (Menakongka & Suthiphongchai 2010). Similarly, stromal cell–derived factor-1, through activation of its receptor chemokine (C-X-C motif) receptor 4 (CXCR4), induced CCA cell invasion via ERK 1/2 and Akt (Leelawat et al., 2007). This process was disrupted by the CXCR4 inhibitor AMD3100 (Leelawat et al., 2007).
Extracellular matrix (ECM) degradation and remodeling is required for tumor progression. MMPs degrade and remodel the ECM during fibrogenesis and carcinogenesis. MMP1, MMP2, MMP3, and MMP9 are strongly expressed in CCAs and are associated with invasive tumors (Prakobwong et al., 2010). Fibroblast activation protein is a stromal protein; its high expression by CAFs has been associated with tumors with an aggressive phenotype (Cohen et al., 2008).
The exact mechanisms by which tumor and stroma communicate are not clear. However, the importance of the desmoplastic stroma in CCA progression indicates that it could be a new therapeutic target, perhaps via selective targeting of CAFs (Mertens et al., 2013).