CTHRC1 mediates multiple pathways regulating cell invasion, migration and adhesion in glioma

Recently, collagen triple helix repeat containing-1 (CTHRC1) has been reported to be increased in several types of human solid cancers and to be associated with tumor invasion and metastasis. However, the expression and function of CTHRC1 in glioma have not yet been reported. In the present study, we investigated whether CTHRC1 plays a role in glioma pathogenesis. Using the tissue microarray technology, we found that CTHRC1 expression is significantly increased in glioma compared with tumor adjacent normal brain tissue (P<0.01, χ² test) and increased CTHRC1 staining was associated with WHO stages (P<0.05, χ² test). The mRNA and protein levels of CTHRC1 were significantly upregulated in human primary glioma tissues (P<0.001, χ² test). We also found that CTHRC1 was significantly increased in glioma cell lines compared to normal human astrocytes (P<0.01, χ² test). Furthermore, Knockdown of CTHRC1 suppressed glioma cell invasion and inhibited enzyme activity of MMP-2. Moreover, our data showed that knockdown of CTHRC1 inhibited glioma cell migration and adhesion capacity when compared with the control cells, and CTHRC1-siRNA reduced the levels of phosphorylated Src and FAK protein expression. Taken together, this study suggests that CTHRC1 plays a role in glioma development and progression by regulating invasion, migration and adhesion capabilities of cancer cells.