β1
integrin (ITGB1) is the major expressed
integrin protein of normal cells and
tumor-associated cells. It is often up-regulated in human
malignancies and is involved in many developmental processes, such as
tumor progression and
metastasis. However, little is known about the function of ITGB1 in
colorectal cancer. We constructed lentiviral vectors expressing ITGB1 or ITGB1-specific RNA interference (RNAi) and an unrelated control vector. After infecting HT29 cells in vitro, proliferation and migration were evaluated by Cell Counting Kit 8 (CCK-8) assays, transwell invasion assays, and Western blots. The influence of
lentivirus infection on the
tumor development capacity of HT29 cells in vivo was examined by
xenografting the
tumor cells. The expression of ITGB1 in the xenografted
tumor cells was analyzed by immunohistochemistry. The up-regulation of ITGB1 significantly increased the proliferation in HT29 cells in vitro. Moreover, we found that the overexpression of ITGB1 up-regulated sonic hedgehog (Shh) while down-regulating Gli1 and SuFu in HT29-ITGB1 cells compared to controls. Moreover, the levels of c-myc and
cyclin D1 proteins were up-regulated. Transwell assays showed that the number of migrating HT29-RNAi cells was lower than that in the other cell groups, indicating that ITGB1 significantly enhances the invasive ability of HT29 cells. In addition to these in vitro results, ITGB1 was found to be a significantly effective
growth factor in a xenografted
tumor mouse model. These results suggest that ITGB1 induces growth and invasion in a human
colorectal cancer cell line through the hedgehog (Hh) signaling pathway in vitro and in vivo.