Focal adhesion kinase (FAK), which plays a pivotal role in mediating cell proliferation, survival and migration, is frequently overexpressed in human
colon cancer. In the present study, we utilized the
short hairpin RNA (
shRNA) to knock down the expression of FAK in SW480 human
colon cancer cells in vitro. Furthermore, nude mice bearing human colon
carcinoma SW480 were established and treated with plasmids encoding FAK
shRNA encapsulated in
DOTAP: Chol cationic
liposome through tail vein injection.
Tumor growth and potential side effect were observed during the treatment. Assessments of angiogenesis, cell proliferation, and apoptosis were performed by using immunohistochemistry against CD31,
proliferating cell nuclear antigen (
PCNA) and TUNEL assays, respectively. The results indicated that
DOTAP: Chol could efficiently deliver the therapeutic plasmids systemically to
tumor xenografts, resulting in suppression of
tumor growth. Treatment with plasmid encoding FAK-targeted
shRNA reduced mean
tumor volume by approximately 86% compared with control groups (p < 0.01), accompanied with angiogenesis inhibition (p < 0.05),
tumor cell proliferation suppression (p < 0.05) and apoptosis induction (p < 0.05). Taken together, our data demonstrated that
shRNA-mediated silencing of FAK might be a potential therapeutic approach against human colon
carcinoma.